Lectures of the Diagnosis of Diseases of the Brain: Delivered at University College Hospital

Google

This is a digital copy of a book that was preserved for generations on library shelves before it was carefully scanned by Google as part of a project

to make the world's books discoverable online.

It has survived long enough for the copyright to expire and the book to enter the public domain. A public domain book is one that was never subject

to copyright or whose legal copyright term has expired. Whether a book is in the public domain may vary country to country. Public domain books

are our gateways to the past, representing a wealth of history, culture and knowledge that's often difficult to discover.

Marks, notations and other maiginalia present in the original volume will appear in this file - a reminder of this book's long journey from the

publisher to a library and finally to you.

Usage guidelines

Google is proud to partner with libraries to digitize public domain materials and make them widely accessible. Public domain books belong to the
public and we are merely their custodians. Nevertheless, this work is expensive, so in order to keep providing tliis resource, we liave taken steps to
prevent abuse by commercial parties, including placing technical restrictions on automated querying.
We also ask that you:

+ Make non-commercial use of the files We designed Google Book Search for use by individuals, and we request that you use these files for
personal, non-commercial purposes.

+ Refrain fivm automated querying Do not send automated queries of any sort to Google's system: If you are conducting research on machine
translation, optical character recognition or other areas where access to a large amount of text is helpful, please contact us. We encourage the
use of public domain materials for these purposes and may be able to help.

+ Maintain attributionTht GoogXt "watermark" you see on each file is essential for in forming people about this project and helping them find
additional materials through Google Book Search. Please do not remove it.

+ Keep it legal Whatever your use, remember that you are responsible for ensuring that what you are doing is legal. Do not assume that just
because we believe a book is in the public domain for users in the United States, that the work is also in the public domain for users in other
countries. Whether a book is still in copyright varies from country to country, and we can't offer guidance on whether any specific use of
any specific book is allowed. Please do not assume that a book's appearance in Google Book Search means it can be used in any manner
anywhere in the world. Copyright infringement liabili^ can be quite severe.

About Google Book Search

Google's mission is to organize the world's information and to make it universally accessible and useful. Google Book Search helps readers
discover the world's books while helping authors and publishers reach new audiences. You can search through the full text of this book on the web

at |http: //books .google .com/I

1^

?"

LECTUEES

BIAGNOSIS OF

DISEASES OF THE BEAIN

DSUFERBD AT UNirBRSITY COLLSOE HOSPITAL

■ tf V BY

W/E> eOWEES, M.D., F.E.O.P.

LONDON

J. & A. CHUECHILL

11. NEW BUBLINGTON STREET

/jrJ4,e. 35.

PREFACE.

-•*-

Many readers of my " Diagnosis of Diseases of the Spinal
Cord" have asked me for a book, similar in scope and
method, dealing with the symptoms and methods of
diagnosis of Diseases of the Brain. In response to that
request, I publish these Lectures, delivered at University
CoUege Hospital.

I have left the Lectures very much in the form in which
they were delivered, believing that thus they will be most
useful. The account of the diagnosis of the nature of the
lesion, contained in the concluding Lectures, is intended
rather to impress on the student the methods of diagnosis
and the most important distinctions between the various
diseases, than to furnish an exhaustive description of these
distinctions. At the same time, I believe that those given
will enable a diagnosis to be made in the majority of the
cases that the student or practitioner is likely to encoimter.

Queen Anne Street, London,
Jwri/et 1885.

CONTENTS.

-•*-

LECTURE I.

iNTRODrcTiON. — The Elements of the Brain, 1 ; Secondary Degeneration, 3 ;

Results of Experiment, 3 ; Relation of Cells and Fibres, 4 ; Centres, 5.
Medical Anatomy. — Convolutions, 7 ; Structure of Cortex, 8 ; Motor

Centres, 10 ; Motor Path, 13 ; Sensory Path, 15 ; Sensory Centres, 16 ;

Illustrative Case, 17.

LECTURE 11.

Medical Anatomy (drntirmed). —Visual Path, 18, Centres, 21 ; Half-
Vision Centre, 22; Higher Visual Centre, 23; Olfactory Path, 24.
Auditory Path, 24. Path of Taste, 25. Paths of the other Cranial
Nerves, 26. Nerves of Medulla, 27 ; Auditory Nerve, 28 ; Sixth and
Facial Nerves, 28 ; Fifth Nerve, 29 ; Third Nerve, 29 ; Fourth Nerve, 30 ;
Relation of Nerves to Motor Tract, 31.

LECTURE III.

Medical Anatomy (Continued). — Fibres between the Cerebrum and Cere-
bellum, 32 ; Central Ganglia, 35 ; Middle Lobe of Cerebellum, 36 ;
Olivary Bodies, 37.

Blood- Vessels of the Brain. — Arteries, 37, of Central Ganglia, 38, of
Cortex, 40, of Pons and Medulla, 41. Venous Circulation, 41.

LECTURE IV.

Symptoms of Brain Disease. — Mechanism of their Production, 44 ; De-
struction of Tissue, 45; Ansemia, 46; Irritation, 46; "Direct" and
" Indirect " Symptoms, 48.

Motor Symptoms, 49 ; Hemiplegia, 50 ; Affection of Muscles according to
Unilateral or Bilateral Use, 52, of Automatic and Voluntary Move-
ments, 53, of Movements effected by Non-corresponding Muscles, 53 ;
Reflex Action, 54 ; Rigidity, 54.

LECTURE V.

Motor Symptoms {C&nMnvM), — Hemiplegia (CorUiniied) : Nutrition of the
Muscles, 56 ; Vaso-motor and Trophic Changes, 57 ; Mode of Recovery, 57 ;
Varieties, 58 ; Subsequent Disorders of Movement, 59.

Convulsions. — Mechanism, 61 ; Form, 62 ; Weakness after, 63 ; Signifi-
cance of Character, 63 ; Exciting Causes, 64. Hysteroid Convulsion, 65.
Other Forms of Spasm, 66. Inco-ordination, 66.

CONTENTS.

LECTURE VI.
Senbohy Symptoms. — Hemianffistlioaia, 87; Partial Losb, 68; Hyaterica.1

HeiaiancestheBia in Organic Disease, 69 ; Sensory Irrit&tiou, 70.
Crasial Nbhves. — Olfactory, 72; Optic, 73; Croaaed Amblyopia, 74:

Hemiopia, 74 ; Mode of Examining Vision, 75 ; Varieties of Heiuiopia, 79 ;

Transient Lobs of Sight, 60 ; Irritation -Symptoms, SI.

LECTURE VII.
Ckanial Nerve Symptoms {CmiUnued). — Motor Nerves of tlie Eyebal), 82 ;
Doulile Vision, 83 ; Projection of Vianal Field, 84 ; Paralysis of Individnal
Mnscles, 86, of Individual Nerves, 88 ; Paralysie of Intra-ocnlliv Musclag,
8fl, Fifth Nerve, 90. Facial Nerve, 91.

LECTURE VIII.
Cranial Neeve Symptoms {Gontinved). — Auditory Nerve, 94 ; Deafness, 95 ;
Tinnitos, 97. Gloaso -pharyngeal and Pnenmogaatric Nerves, 98 ;
Paralysis of the Pharynx, 88, of tho Larynx, 99, of the Palate, 103.
Hypoglossal Nerve, 106 ; Impairment of Articalatjan, lOS. Associated
Palsies of Cranial Nerves, 108.

LECTURE IX.

LECTURE X.
ArEECTioNB or SrBBon.^MochaniBma Cor Speech, 120; the Expitsaion of
Emotion and Ideas, 122 ; Motor and Sensory Relations of Speech, 123 ;
Parts of the Brain concerned, 124 ; the Sight Hemisphere and Speech,
125 ; Characters of Defect of Speech, 137 ; Motor Aphasia, 129 ; Origin
of Errors in Utterance, 131 ; Loss of Writing, 134 ; Defective Revival of
Words— Verbal Amnesia, 134 ; Word-Deaf iiesa, 13fi ; Inability to Read,
137. Recapitulation, 137. Testamentary Capacity, 139.

LECTURE XI.

Symptoms [Continved). — Headache, 140. Other Cephalic Sensations, 143.
Vertigo, 145 ; Varieties, 148. Vomiting, 150,

LECTURE XII.
STMPTOMa (CoJlWtitKii?).— Temperatnn

Vaso-motor Diaturbanco, 168 ; R<

of the Sphincters, 163.
Ophthalmoscopic Chanoes.— Associated, 159 ; Consecutive, 159 ; Neuritis,

160 ; Atrophy, 16G ; Circulation in tho Brain and Eye, IBS.

CONTENTS. VU

LECTUEE XIII.

Diagnosis of the Seat of the Disease. — "Localization," 167; Preliminary
Questions, 168 ; Symptoms of Disease of the Frontal Lobe, 170, Central
Region, 171, Parietal Lobe, 172, Occipital Lobe, 172, Temporal Lobe,
172, Island of Reil, 173, White Substance, 173, Central Ganglia, 173,
Internal Capsule, 174, Corpora Quadrigemina, 175, Cms Cerebri, 175.

LECTURE XIV.

Local Diagnosis {Continued), — Symptoms of Disease of the Pons Varolii,
176, Medulla Oblongata, 178, Middle Peduncle of the Cerebellum, 179,
Middle Lobe, 179, Hemisphere, 180.

Review of Symptoms in Relation to Locality. — Hemiplegia, 180 ;
Paralysis of Cranial Nerves, 182 ; Symptoms of Disease of the Base, 183.

LECTURE XV.

Diagnosis of the Nature of the Lesion. — ^Diagnostic Pathology:
Congestion of the Brain, 186 ; Cerebral Haemorrhage, 187 ; Softening of
the Brain, 190 ; Thrombosis in Sinuses, 192 ; in Veins, 193 ; Injury to
the Brain during Birth, 197 ; Meningitis, 198 ; Tumours, 199 ; Abscess,
200 ; Relation of Symptoms to Morbid Processes, 201.

LECTURE XVI.

Pathological Diagnosis {CoiUimied). — Sudden Lesions: Premonitory
Symptoms, 205; Onset, 206; Causal Indications, 207 ; State of Heart, 207;
Syphilis, 208 ; Vascular Degeneration, 209 ; Evidence of similar Lesions
elsewhere, 211 ; Position of Lesion, 212.

LECTURE XVII.

Pathological Diagnosis [Contimied). — Chronic Lesions: Age, 215;

Heredity, 216 ; Diffuse Symptoms, 217 ; Focal Symptoms, 219.
Review of Symptoms due to the several Lesions. — Congestion of the

Brain, 220 ; Meningeal Hsemorrhage, 221 ; Ventricular Hsemorrhage, 221 ;

Haemorrhage and Softening of the Pons, 221 ; Cerebral Haemorrhage and

Softening, 222 ; Yenous Thrombosis, 223 ; Meningitis, 224.

LECTURE XVIII.

Pathological Diagnosis ( Continued).— Chronic Meningitis, 226 ; Tumour, 227 ;

Abscess, 229 ; Aneurism, 230 ; Labio-glossal Paralysis, 232 ; Insular

Sclerosis, 232 ; General Paralysis of the Insane, 233.
Diagnosis — Distinction between Functional and Organic Diseases, 233 ;

Hysterical Palsy, etc., 235.
Conclusion, 237.

THE

DIAGNOSIS OF DISEASES OF THE BEAIN

LECTUEE I.

INTRODUCTION— MEDICAL ANATOMY OF THE BRAIN ; CORTEX,

MOTOR PATH, SENSORY PATH.

Q-ENTLEMEN, — The subject of the diagnosis of diseases of the
brain certainly transcends in complexity, and perhaps exceeds
in interest, all other problems in practical medicine. In .
nerve-elements the involution of energy reaches the highest
degree known to us, and in the chief organ of the nervous
system these elements, vast in number, various in character,
are arranged in what seems to us extreme complexity. The
number of the nerve-cells of the brain is not known, and if it
were, our minds would be powerless to grasp the extent of the
array. The cortex alone has been estimated to contain eight
hundred millions of cells. Of all the elements that compose
the brain, not one is isolated. Each is connected with others,
and their anatomical connection subserves a corresponding
functional association. A change in the functional state of
one involves a change in the functional state of others ; and
change is constant, rest unknown.

Complex as the arrangement of the elements of the brain
appears to us to be, it may be found, with fuller knowledge,
that the principles of the plan are comparatively simple. The
variety in form of the nerve-elements is small, if we consider
how nimierous they are. The fibres present little variation.
The cells, even when the element of size is taken into con-

B

k

sideration, may probably be olassed in not more than a dozen
varieties. It is the arrangement and connection of these
elements that constitutes the complexity of structure of the
brain, and subserves its complexity of function. At the same
time we must remember that the varieties of form give ua no
clue to the difPerenees that may exist among the elements
of which nervous tissues consist. Neither microscopical
examiuation uor chemical aualysifi can penetrate beyond the
coarsest outlines of the constitution of hving matter. It is
probably within the facts to assert that each nerve-cell
contains as many material atoms as the brain contains
nerve-cells. Even the moleoides, formed by the grouping
of these atoms, are beyond the reach of any means of
scrutiny we possess, or of which we have, at present, any
promise. The fundamental diversity that must exist, where
we can discern only uniformity, is shown to us by the
action of poisons, and in the effects of disease. One poison
acts on one part of the nervous eystem, and leaves un-
influenced another part, which a second poison affects alone,
"We are accustomed to explain this by the difference in the
chemical constitution of the poison ; but it is evidence of an
eqasi difference in the nerve-elements, that are, as we say,
" selected " by it. The selection is no matter of arbitrary
choice. It is the result of the nature of the nerve- elements
themselves ; the expression of differences between them,
revealed by such effects alone. This consideration renders
many effects of disease more inteUigible, though it may not
lessen their mystery.

Certain leading facts regarding the structure of the
brain must be clearly recognized, if we would understand
what is known of the principles of the diagnosis of its
diseases. Our present knowledge of the cerebral structure is
at once far more thau we can use, and far less than we need.
The researches of the last quarter of a century — of Lockhart
Clarke, Broadbent, and others, in this country; of Stilling,
Meynert, Wernicke, Flechsig, among the Germans ; of Luys,
roville, and others, in France— have brought to light an

INTRODUCTION. d

immense number of facts, and have built up a large mass
of knowledge, much of which has at present no practical
application.

But if we attempt to select from the facts described by
different investigators those that are of chief importance, we
are at once met by a fresh difficulty. Many of the conclu-
sions reached by different investigators do not correspond, —
are even contradictory. This is not surprising. The inter-
lacing tracts of fibres baffle the scalpel, and even the
microscope, when we attempt to trace their course. What,
then, is to be our guide when investigators disagree ?
Fortunately we are not dependent only on simple dissection,
or even microscopical examination. The selective action of
disease affords invaluable help in the study of the structure
of the nerve-centres. It was long ago discovered (by Waller)
that if nerve-fibres are destroyed at a given point, they
undergo degeneration beyond th^ lesion, and this degenera-
tion extends along them as far as they continue simple fibres.
The degeneration is only in one direction, and that is the
direction of functional conduction ; on the side of the lesion
from which the fibre conducts there is no degeneration. By
means of this "secondary degeneration" the course of some
tracts of fibres may be traced with precision through the
brain. Moreover, we have a second guide. A distinguished
German investigator, Fleohsig, has availed himself of the
fact that different tracts of nerve-fibres in the brain acquire
their white substance at different stages of foetal and infantile
life. He has shown, by a remarkable series of investigations,
that we may learn as much of the course of fibres by studying
them in their birth as in their death — in their development
as in their decay. His discoveries have thrown new light on
many difficult problems, and supply a trustworthy guide in
discovering where the truth lies in other and contradictory
descriptions.

The experimental researches on the functions of the
brain, chiefly of Hitzig and Munk in Q-ermany, and
Ferrier in this country, have also given us vast help
in diagnosis. Here also, however, we meet with con-

B 2

tradiotions ; and here also more has been asoertained than
we can at present apply. Our guide in this department
must be the faots of clinical and pathological observation.
"We must beware of applj-ing wholesale to the human brain
the conelusiona derived from experiments on animals. The
latter are of value fo us only as indieationa for observation on
man, and by enabHng us to give a fuller interpretation to
the facts we leom by our study of disease during life and
after death. Some of the experimental facta have at preaenfc
received no confirmation, and on some points we especially
need information, which, from their nature, experiment
cannot give.

Before we enter on those details regarding the atnicture
and functions of the brain that are of chief importance
for diagnosia, I must remind you of certain important ele-
mentary facts. We speak of nerve-cells and nerve-fibres as
if they were merely connected stnictnres, essentially distinct.
They are not really ao. The axis-eyHnder of each nerve-
fibre is the prolonged process of a nerve-cell, sharing all
changes of nutrition that the nerve-cell undergoes, suffering
with it when the cell is damaged. This is the secret of the
secondary degeneration. If a fibre, or part of a fibre, is cut
off from its parent cell, it degenerates; the part still in
connection with the cell does not degenerate. If the cell is
destroyed, the whole fibre perishes. Although I have said
that every fibre is a nerve-cell process, I need hardly fell
you that the fact is not proved. It never can be proved by
observation. But the relation can be observed of some cells
in various parts of the nervous ayatem ; the contrary has
never been observed ; and we may therefore infer, with con-
siderable probability, that the fact is true of all nerve-fibres.
We do not know whether any nen-e-fibres unite directly the
undivided processes of two nerve-cells. It is highly probable
that, aa a rule, they do not, because we usually find that only
one pi-oeess of a cell becomes directly an axis-cylinder ; the
other processes divide and ramify in a hrancliiug network
of the finest nerve-fibrillBB. This structtire is probably

INTRODUCTION CENTRES. O

intermediate .between adjacent nerve-cells, and in it the
nerve-fibres may end, that are the prolonged processes of
other and sometimes distant nerve-cells.

Another preliminary consideration is of a different nature.
It is necessary, in speaking of the functions of the brain, to
use the term " centre." Eemember that the word is employed
in its physiological sense ; not in a geometrical, or even in a
topographical, sense. It indicates a combination of nerve-
cells subserving a given function. Note, first, that this
function may not be the only one subserved by the group of
nerve-cells. In many groups the nerve-cells are very numer-
ous; they are connected with Qach other by a ramifying
plexus of fibrillsB, and are connected with other and distant
groups of cells by nerve-fibres. Such a collection of cells may
contain many centres, since only some cells are probably in
action at the same time. The possible functional combinations
in such a group are almost infinite, since the variations involve
not only the number of cells in action, but the relative degree
of their action. Only some of these are usually, perhaps ever,
in functional activity. Lines of various resistance exist by
which the functional combinations are determined. Education
is largely the establishment of these lines ,of least resistance.
Habit depends upon them. Although the finest, most com-
plex mechanism of human contrivance is rude compared
with the simplest arrangement of the brain, I may illus-
trate this variation of function by an object with which
you are all familiar. Wherever large buildings are being
erected, or Extensive excavations made, you will see a
steam crane. This machine, by a change in the relation
of the different parts of the complex mechanism, may be
made either to draw up a weight, to swing itself round, or
to travel along a line of rails. The motive force is the same
— the machinery is essentially the same ; the difference in
result depends on certain parts of the machinery being in or
out of "gear." In the one machine are functional centres
for progression, rotation, and turning a windlass.

Not only may one part of the brain contain many centres,
but a single functional centre may consist of nerve-elements

(J LECTURE I.

tlidt aro anatoniioally distant — even situated in different
lioniiHpheroH. Cells may act together when the nerve-fibre
tlial- (jouuoots them is many inches long, as perfectly as if
thoy aro only a hundredth of an inch apart, just as the
uoeMllort of two galvanometers in the same circuit are deflected
at tht^ same moment, judged by ordinary standards, whether
thoy are distant a foot or a mile.

Olio more preliminary consideration. A familiar line
asHorts that " things are not what they seem," and although
the Hlatoment is scarcely of the imiversal application that its
form sxiggests, it is one that should not be forgotten when we
8t\uly the aiTtmgement of the nervous system. The course
of norve-flbres is often very different from that suggested by
the tH)urao of the nerves in which they run, and the arrange-
ment luul connection of the elements of the brain is often
not the same as that suggested by the coarse morphological
rolrttious of its parts. Nerve-fibres frequently take a course
wot only very different from that which might be anticipated,
but mysterio\idy tortuous, — I was going to say unnecessarily
ti>rt\ums. Doiibtless these irregularities have had their neces-
^ty ; b\it this lies in the dim past of development, beyond
o\ir nuigt> of vision. The course of the fibres of the cranial
norvi^ ivffords nianv illustrations of these anomalies. A
innnj^w^tively simple instance is presented by the spinal part
of tlio spiuivl aooessi^ry nerve, which arises from the same grey
matter asi the cerN-ioal nerves is distributed to the same
mus^^h^ but has a innvrse that takes it just within the
eutrauiv to the cranial w^A-ity, although it has no business
then\ as far as we emi see, to justify its ascent. The course
of the tibres that subser\"e taste is a more elaborate instance
i>f the same thing, and it has caused difficulties fnc^m which
lUMther anatomical nor phA'siological investigation has yet
elearvnl our knowledge.

I mav safely asstmie, gentlemen, that you aie fismiiliar
with the chief facts in the toiK>graphical anatomy of the
Waru, and amOiH^ them with the names of the e»-^nvolutions.
Bii:, as 1 shall have frequently to refer to these, I put before

CONVOLUTIONS.

you a diagram on which the fissures and ooQVolutious are
shown and designated,

I need only add one fact to those that are indicated on the
diagrams. There is, as we shall see, an important difEerenoe

in function between the ascending frontal and the three other
frontal convolutions. Hence it is often convenient to speak
of the latter without the former. We do so by terming the
three antero-posterior convolutions, and corresponding inner

surface, tbe " prefrontal lobe." Thus we mean by thiB term
the portion of tbe brain anterior to the ascending frontal
convolution. It is, like many others, an inaccurate word, but
it has become current, and is convenient — indeed, necessary.

The cortex of the cerebral hemisphere coverB, as you know,
a mass of white substance — the centrum ovale. The cortex
consiste of nerve-eells, with fibres connecting them, aud pro-
ceeding from them to tbe white substance beneath. The cells
vary much in form and size, and certain kinds of cells pre-
ponderate at different depths from the surface, thus enabling us
to distinguish certain layers (see Fig. 3}, which are, however,
ill-defined, and difEer somewhat in different parts of the cortex.
Hence various descriptions of these layers have been given
by different observers. At the surface is a narrow "super-
Jioial layer,"* with few nerve- elements, and beneath this is
a layer of small pijrmnidal cells densely massed together.
Below tbiw is a thicker layer of large pyramidal cclh, which
are larger in the deeper than in the more superficial part
of the layer. The apex of the pyramidal cells is tamed
towards the surface. Next comes a layer which contains still
larger ceUa, some pyramidal, and others more irregular in
form, and, from the resemblance of the latter to the cells of
the anterior comu of the spinal cord, this layer is termed the
gaitglion-cell layer. In the motor region of the cortex these
oeUa are especially large, many of them exceeding in size
any other cells in the nervous system. But between this
layer and the last, or rather in the lowest part of the last,
the large pyramidal layer, small round or angular bodies are
rather numerous ; and over a considerable part of the cortex,
especially that in which the sensory functions seem chiefly
developed, these increase in number, and constitute a weU-
marked granuk layer. Beneath the ganglion-cell layer, and
next the white substance of the hemisphere, is a layer in
-wiack fusiform eelh preponderate.

The white substance consists of fibres passing in various

directions. Some pass from one part of the cortex to another

* The italics indicate the namea coniiiiouly given to the layers.

/IW AumerlitHt

The drawiDgs were made
^m sectiaoa of the ascend-
ing frontal and first snnee-
tant coDTolutions (the latter
□ear the eitremtty of the
parieto - occipital fiaanre).
The aeetioiiB were kindly
furnished me, aa representa-
tive of the so-called motor
and sensory types, by Dr.
B«van Lenis, whose import-
ant investigationB into the
Btmcturs of the cortei are
well known. In addition to
the beta mentioned in the
text, certain others may be
noted. No layer is composed
exclusively of one kind of
cell ; most fonns are met
with in each layer, but some
are scarce and others abun-
dant. Almost all the pyra-
midal cells have their apex
turned towards the surface of
thebrain. The granule layer
of the sensory type is formed
at the expense of the two
adjacent layers, the large
pyramid layer and the gan-
glion-cell layer, and these
two layers in the motor typo
merge one into the other to
an even greater degree than
the other layers. In the
sensory type the very large
ganglion cells of the motor
type are absent. Inthewhife
substance, nuclear bodies lie
among the fibres, and near
the grey cortex isolated
occur, similar to those in the
grey matter, becoming few as
we pass more deeply into the
white substance. Many fibres
run through the grey sub-
stance towards the surface,
and they are, to ;
aggregated into bundles, par-
tMlly separating the nerve-
cells into colunms. To avoid
con fusion these fibreahave not
been shown in the diagram.

^-■;'-u'/^ '.'4i%' ^"f*" '^n'^v' *'"''- ';^"-''' 'fl

III »i

W

mi

if

III

m

nh

Im

10 LECTURE I.

part in the same hemisphere. Others pass inwards to the
corpus oallosum, and probably, through these, corresponding
parts of the two hemispheres are connected, and brought into
functional unity. Others, from ahnost all parts, converge to
the internal capsule, and to the optic thalamus ; while from
the posterior and under part, fibres pass to the cms, and from
the posterior port, to the corpora geniculata, quadrigemina,
and optic tract.

In our survey of what may be termed the functional
anatomy of the brain — the consideration of the structural
arrangements that subserve special functions— we may pass
next to the parts concerned in voluntary motion. As you
already know, in only one part of the cortex can we trace a
special relation to voluntary motion. This part consists of the
two (so-called " central ") convolutions that bound tbe fissure
of Ilolando, the ascending frontal and ascending parietal,
with the expansion backwards of the latter in the " superior
parietal lobuJe," and also with the medial aspect of these
convolutions on the inner side of the hemisphere — the " para-
central loLule," and part of tbe "precuneus" (Pig. 2). As you
have also learned in the class of physiology, voluntary motion
is not uniformly relat-ed to this region. The leg is chiefly
represented in the upper third of these convolutions, the arm
in the middle third, the face in tbe upper part of the lower
third, the tongue and lips in the lowest part of the ascending
frontal (Fig. 4). Voluntary speech is related to this centre
for the tongue and bps, and to the adjacent part of the third
(lowest) frontal convolution.

We do not know whether there is any sharp limitation
between these Umb-centres ; probably there is not, at any
rate between the centres for the arm and for the leg. In
animals certain movements have been found specially excit-
able at certain points, and representations of the human brain
are often given, to which these centres have been trans-
ferred. But clinical facts have not at present confirmed in
man the existence of these limited centres for certain move-
ments. In animals, moreover, centres are found on the

MOTOR CENTRES.

11

posterior parts of the first and second frontal convolutions.
These are not only unconfirmed so far as the human brain
is concerned, but the balance of evidence is against their
existence.*

This region of the cerebral cortex is certainly motor, but
it is certainly also not exclusively motor. Its destruction by
disease causes persistent paralysis, corresponding in distribu-
tion to the part destroyed ; irritation of it causes convulsions,
that begin in the limb corresponding to the part irritated.

Fig. 4. — Cortical Centres : Left Hemisphere.
The position of the limb-centres is indicated by the letters composing their
names. T, tongue-centre. The dotted line encloses the motor speech-
centre. F L, frontal lobe ; P L, parietal lobe ; L, occipital lobe ; T L,
temporal lobe; /. R, fissure of Rolando ; /.s.a., anterior limb of the
fissure of Sylvius ;/. 5.^., posterior limb of the same fissure;^.©./.,
parieto-occipital fissure.

But destruction of these parts causes also some loss of
sensation, chiefly in the extremity of the limb most paralysed,
and accompanied by an inability to recognize the position of
the extremity, hand or foot — an inability which may be out
of all proportion to the loss of cutaneous sensibility, and
even, strangely enough, may exist alone. Of this peculiar

* Schafer and Horsley find, in monkeys, centres for the trunk muscles in
the highest part of the motor region (especially on the inner aspect), and in
the posterior part of the first frontal convolution. Ferrier found centres for
the movement of the head and eyes on the first and second frontal.

losB I ahall have more to say hereafter. Another fact of
simOar significance is that convulsions produced hy disease in
this region often commence hy a sensory " aura."

Fig. 5.— Diaqkam of thk Cohrhb of the Motor Tract ah shown in

A DIAOBAMMATIO HORIZONTAL SEITION THBOTJSH THE CeREBKAL

Hemisphere, Pons, and Medulla.
Fr, frontal lobe ; Oc, occipital lobe ; A F, ascending frontal, and A P, aacend-
iug parietal convolutious ; F C F, precenh'al fissure in front of the
aBceading frontal couvolutioD ; I P F, interparietal fisaore. A section of
the orura ia lettered on the left aide : S N, subatantia nigra ; Py,
region occupied by the pyramidal librea [motor tract), which on the right
are ahown as coutinnoUB lines, converging in the white subatance of the
hemisphere, to pass through the posterior limb of I C, the internal capsnle
(the elbow of which is sliown at ') — throngh the crua and pons,
and to divide in the medulla into the decussating lateral pyramidal tract
(Ijit), and the non -decussating or anterior pyramidal ti'act (apt).

Prom this motor region of the cortex, fihres pass down to
the spinal cord, and conduct the motor "impulaes," as we

a

MOTOR PATH.

13

call tliem, from the motor mechanism of the convolutions
to the motor mechanism of the grey matter of the cord.
Leaving the cortex, these fibres pass through the white eub-
Btanee of the hemisphere, converging to the " internal cap-
sule," which, as you know, lies between the lenticular nucleuB
(or extraventrieular part of the corpus striatum) on the

The section through the convolutions is vertical ; that through the internal
capsule, I C, horizoDtol ; that through the cms is again vertical. C N,
caudate nucleus ; TH, optic thalamus ; L 2 and L 3, the middle and
outer parts of the lenticular nucleus ; /, a, I, face, arm, and leg ftbrea.
The words in italics indicate the correapoading cortical centres.

outside, and the caudate nucleus, and optic thalamus, on
the inside. Thence the fibres pass into the eras, through
the anterior part of the pons, and constitute the anterior
pyramids of the medulla. Crossing for the most part in
the decussation of the pyramids, they continue down the

cord, where we haye seen tliem as the pyramidal tracts,*
lateral and auterior. This is a loug course ; the longest of
any fibres of the central nervous system. It was formerly
thought that this course was broken in the grey matter of
the corpus striatum ; but this seems to be an error. The
cells of the corpus striatum have no direct relation to
voluntary movement ; the motor tract passes in an unbroken
course from the cortex down to the grey matter from which
the motor nerves directly proceed.

Certain points in the arrangement of the fibres must be
noticed. They do not constitute the whole of the internal
capsule. In horizontal section (Fig. 5) this capsule seems to
consist of two obhque parts, which join at an angle ; the
anterior segment, or " limb," as it is termed, hes outside the
body of the caudate nucleus, the posterior outside the optic
thalamus, and the angle or "elbow" (the "Knie" of the
Gtermaus) lies between the thalamus behind, and body of the
caudate nucleus in frout. The motor fibres occupy only
the elbow and the anterior two-thirds of the posterior
segment. The posterior third of this, as we shall see,
contains sensory fibres, and the anterior segment contains
fibres of uncertain function, which pass down from the
frontal lobe to the cerebellum. "We shall retiim to these
in a subsequent lecture. The fibres from each limb-centre in
the cortex keep together in the internal capsule, but the
several groups exohange their vertical relation for one that
is antero-posterior (Fig. 6) ; the fibres for the face, and
probably for the tongue, occupy the elbow of the capsule,
then come the fibres for the arm, and, most posterior, next
to the sensory fibres, come the fibres for the leg.

From the internal capsule the fibres descend into the cms,
lying in the anterior or lower division (orusta) , and occupy-
ing the middle two-fifths of this region, but separated by
some other fibres from the locus niger above them. To their
inner side lie the fibres that formed the anterior limb of the
internal capsule, and f-o their outer side is another bundle of
fibres, of which I shall have more to say. The relative
• " Diagnosis of DiaeBBes of the Spinal Cord, " 3rd Ed., p. 10.

i

MOTOR PATH SENSORY PATH. 16

arrangement, which was vertical in the cortex, and antero-
posterior in the capsule, here becomes transverse (see Fig. 6),
the fibres for the face lying to the inner side, and those for the
leg to the outer side, of the fibres for the arm. The fibres
for the tongue probably lie close to those for the face.
The latter two sets of fibres leave the others in the pons, and
cross the middle line to the nuclei from which the facial and
hjrpoglossal nerves proceed.

We know much less of the sensory path. Even in the
spinal cord it is uncertain. The older theory (of Brown-
Sequard) , that sensation is chiefly conducted in the grey matter,
is not disproved, but there is reason to believe that some
sensation is conducted by the fibres of the lateral column in
front of the pjn^amidal tract, and by fibres of the posterior
columns. In the medulla and pons the path probably
passes up in the posterior half, above the " fillet," perhaps
chiefly in the curious network of fibres called the " reticular
formation." It has been conjectured that some sensation may
be conducted through the cerebellimi ; but this seems, on the
whole, improbable. The path passes up beneath the corpora
quadrigemina, through the tegmentum of the cms above the
locus niger, and enters the internal capsule, where we are
able exactly to determine its position. It occupies, as I have
already told you, the posterior third of the hinder limb of
the capsule. These fibres were once thought to be the same
as those which, in the cms, occupy the outer fifth of the
crusta ; but Flechsig has shown that this is an error. These
outer crustal fibres radiate into the white substance of the
occipital and temporo-sphenoidal lobes, and connect those lobes
with the cerebellum. As these fibres leave the cms, their
place is taken by sensory fibres from the tegmentimi, which
.thus form the posterior part of the internal capsule. Hence
you will perceive how uncertain is our knowledge of the
greater part of the course of the sensory path. Between
the posterior roots of the spinal nerves and the internal
capsule we have no definite facts regarding its position.
We know only that it crosses the middle line in the spinal

16 LECTURE I.

cord, not far above the level at whicli the nerves ent©
and that it passes up the pons on the same side as that
which it occupied in the cord. In the upper part of the
pons the path from the fifth nerve — from the face, etc. —
joins it, so that the posterior part of the internal capsule
conducts sensation from the whole of the opposite half of the
body and head, skin and mucous raembranea, as far as the
middle Hne. Moreover, the facts of pathology show that the
path of cutaneous sensibiUty is here contiguous to the path of
special sensibility from the organs of special sense — of taste,
hearing, smell, vision — which receive sensory impressions from
the opposite side. Hence Charcot has termed this region
the "sensory crossway." I say "from the opposite side"
rather than "from the nerves of the opposite side," because,
in the case of vision, the impressions that pass by this
sensory region are those which come from the half of each
field of vision corresponding to the side from which the other
sensory impressions come. We shall have presently to
consider this point more folly.

The ultimate destination of the sensory path is still to a
large extent imcertain. Some fibres enter the optic thalamus,
but their function is unknown, as there is not at present any
evidence to show that impressions which influence consciousness
pass through the thalamus, except, perhaps, in the case of
visual impressions. The sensory fibres pass into the white
substance of the hemisphere, and go towards the parietal
and central ("motor") region; roughly speaking, towards
that part of the cortex that lies under the parietal bone
(Fleohsig). We have already seen that disease of the
motor cortex often causes impairment of tactile sensibility ;
and that when convulsions ore caused by disease of this
part of the surface, they often begin with a sensory aura.
Thus clinical evidence, as well as the facta of anatomy, points
to the outer part of the hemisphere in the middle region as
being the part concerned in sensation. A case which has been
recorded by Deraange* shows that the indication is correct,
and places the conclusion beyond doubt. This case is so
•" Revue de Med," May, 1883, p. 391.

M

SENSORY PATH. 17

important that I must mention its leading facts: — A
woman, aged 72, after suffering for two weeks from
tingling and numbness in the left arm and leg, was foimd to
have almost complete loss of sensation of touch, pain, and
temperature in the whole of the left side, face, and limbs ; with
amblyopia and loss of colour-vision in the left eye. (We
will consider subsequently the significance of this loss of
sight.) The mucous membranes were not then anaesthetic,
but a fortnight later were found to have lost sensibility, and
the cutaneous anaesthesia was complete up to the middle line.
Smell and taste were also lost on the left side, and the im-
pairment of vision was greater. There was also considerable
weakness in the left limbs; this gradually increased, and
involved the face and the tongue. These symptoms continued
until death, six months after the onset. An extensive area
of softening was found, involving a large part of the outer
surface of the right hemisphere and subjacent white sub-
stance ; the inner surface of the hemisphere, central ganglia,
and internal capsule were unaffected. The precise area of
cortical damage was — lower two-thirds of the ascending frontal
and ascending parietal, with the posterior extremities of the
middle and lower frontal; island of Eeil, inferior parietal
lobule, superior parietal lobule adjacent to the intraparietal
sulcus, the angular gyrus, and the whole of the occipital
and temporo-sphenoidal lobes on the outer surface. The
softening of the inferior parietal and angular convolutions
seemed of rather older date than that elsewhere.

This case affords a crucial demonstration of the correctness
of the indications afforded by the anatomical researches of
Flechsig. We shall have to return to it again when we
consider the central relations of vision.

LECTUEE II.

MEDICAL ANATOMY OF THE BRAIN (Cordimted) : NERVES OF
SPECIAL SENSE— OTHER CRANIAL NERVES.

Gentlemen, — In our survey of those points in the ana-
tomy of the brain that are of chief medical importance, it
may perhaps be most convenient to study, next, the central
relations of the cranial nerves. We wiU consider first,
however, those nerves that subserve the special senses,
and wiU begin with that which is most difficult, of which
we have most knowledge, and yet (perhaps therefore) see
most clearly how imperfect our knowledge is — the ner\^e
of sight. At the optic chiasma these nerves undergo a
partial decussation, rather more than half the fibres cross-
ing. Fifteen years ago this semi-decussation was regarded
as satisfactorily proved; but in this questioning age few
doctrines seem imassailable, and it has been maintained
that there is a total decussation. The result of the discus-
sion that has taken place is to show that the old doctrine
is correct, and to place it upon a firmer basis. In some
animals there is a total decussation ; but this occurs in those
creatures in which the eyes are so placed that they never
act together, and in which the fields of vision are entirely
separate. In proportion as the two eyes are used to-
gether, and the fields of vision correspond, the fibres
cross, so as to bring the corresponding regions of each

VISUAL PATH.

19

retina into relation with one cerebral hemisphere. In
man the inner half of each field of vision is smaller than
the outer half, because it is limited by the projecting nose.

LF

RF

Fig. 7. — Diagram of the Relation of the Field of Vision, Retina,

AND Optic Tract on each side.

R F, L F, right and left fields — the asterisk is at the fixing point j R R, L R,
right and left retina— the asterisk is at the macula lutea ; hh^ r.hy left
half and right half of each retina, receiving rays from the opposite half
of the field ; R N, L N, right and left optic nerves ; C%, chiasma ; R T,
L T, right and left optic tracts ; below, the halves of the fields from which
impressions pass by each optic tract are superimposed.

Although the two halves of the retina are of equal size,

the sensitiveness of the outer, temporal half (which receives

rays from the inner, nasal half of the field of vision)

c 2

20 LECl'UliE 11.

does not extend so far towiirds the fi-ont as does that of
the inner, nasal half. This is shown by examining the
field — fii-st when the eye ls directed forwards ; secondly,
when it is directed outwards. The limit of the nasal
lialf of the field is nearly the sanie in each case,
although, when the eye is directed outwiu-ds, the nose no
longer outs off the rays. Doubtless the stnicture of tlie
retina corresponds to tliis ; its temporal hnll contains few er
nerve-elements than does the nasal half, and from this half
fewer nerve-fibres proceed. The fibres that decussate are
those from the nasal half of each retina, ami hence the fibres
that cross are more numerous than those that do not ctous
If the fibres from the whole of one retma ha\ e degenerated
tbe opposite optic tract shnnLs n size more than the oj t c
tract on the snnie side D ea t? of ne pt c tract .

Tlici shading represents the blinit part ; the oral oiitlin

tlie a.vei'age normal Held. Tlie asterisk is the iiKiiig point, Tlic small
circle represents the blind spot.

left., therefore, arrests the couduetiou from the same-named
half of each retina, and causes loss of viiion in the opposite
half of each field — "hemiopia," or "hemianopsia," ae it is
termed. {Fig. 8.)

The division between the two half -fields is usually m, or very
near, the vertical line passing through the fiiing point (corre-
sponding to the macula lutea of the retma) Somi times it
pusses thixjugh the fixing point ; more often it diverges and
paflsea round the fixing point, a httle distance from it, to
return again to the middle line, and this whichever side is

oe IS I

VISUAL PATH. 31

'blind. The balance of evidence at present collected seems to
show that this difEerence does not depend on the seat of the
disease causing the hemiopia ; and it can therefore only be
explained by individual difEerencee in the decussation. lu
mauy individuals, it would seem, fibres from a small area
around the centre of the macula pass by each optic tract;
while in some persons, each tract contains fibres from only
one half of the macular region, as it does from the rest
of the retina. Another form of variation seems to show
also that there are considerable differences m the character of
the decussation. Above and below the fixing point, the hne of
division is also often irregular, sometimes, for instance, sloping

off to one side above, and to the other side below, the two fields
corresponding closely. In an extreme example of this, such
as is shown in Fig. 9, the division becomes irregularly oblique
instead of vertical. It is impossible to explain this, except
on the theory of variations in (he decussation. Some facts
suggest that there are similar variations in some other decus-
sations in the nervous system, especially in that of the sensory
tract from the skin.

The visual path passes in the optic tract, by the corpora
geniculata, through the white substance of the hemispheres,
to the cortex of the occipital lobe on the outer surface. If it
is destroyed anywhere in this course, the result is hemiopia
of the some character. Disease of the cortex of the occipital
lobe has a like effect. There is no complementary decussation
at the corpora quadrigemina, as has been fancied. Whether

22 LECTURE II.

the fibres from the tract to the cortex are interrupted by grey
matter, or are continuous, we do not know. Fibres from the
tract enter the external corpus geniculatum, the optic thalamus,
the corpora quadrigemina. Fibres from these pass into the
white substance of the hemisphere, and the grey matter
of these bodies may be interposed in the optic path. It is
probable, however, that the fibres that enter the corpora-
quadrigemina substance only guide the movements of the
eyeball. On the other hand, some fibres from the tract pass
directly into the hemisphere, and these may continue the visual
path, or part of it, directly to the cortex.

The experiments of Munk lead him to believe that in dogs
the anterior half of the half- vision centre of the occipital lobe
subserves the upper quarter of the retina (and therefore the
lower quadrant of the field) ; and the posterior half of the
centre subserves the lower quarter of the retina (and there-
fore the upper quadrant of the field). The frequency of
partial hemiopia in man, c.g.^ the loss of a lower or upper
quadrant, makes it certain that there must be an arrangement
of the fibres and a central representation on a sj^stem similar
to that in the dog, although whether the correspondence
holds good in the details of the plan we do not yet know.

But the central relations of ^dsion are still more complex.
The subjects of that strange disease, hysteria, sometimes suffer
from hemianoesthesia and loss of the special senses on the
anaesthetic side, together ^\'ith — ^not hemiopia — ^but what is
termed " crossed amblyopia," dimness of sight of the eye on
the anaesthetic side, peripheral constriction of the field of
vision, and often loss of colour- vision. There is usually also
a far slighter limitation of the field of the other eye. The
curious s^>inptoms of hysteria probabl}' depend on some morbid
action in high cortical centres. They may teach us much of
the functions of the brain, much of the association of its
elements on which those fimetions depend; although they
furnish no indication of the coarser anatomical relations.
The otx^un^nee of this amblyopia shows that there must be a
functional centime, capable of being inhibited, in which is
represented chiefly the whole field of one eye, not the half-

VISUAL CENTRES. 23

fields of both eyes. It does not, however, show that this field
is situated in one hemisphere, since the half -vision centres in
the two hemispheres might be so connected as to be susceptible
of such combined partial inhibition as would produce the
symptoms. But the experiments of Ferrier have shown that
lesions of the angular gyrus in animals will cause dimness of
sight of the opposite eye, which rapidly passes away. In
rare cases in man, in which there is certainly organic disease,
similar crossed amblyopia has been observed. I have seen a
few instances of this, and several others have been recorded.
Moreover, the case I have quoted (p. 16) is proof that such
amblyopia may result from disease of the outer surface of the
hemisphere. It will be noted that in this case the lesion
involved the occipital lobe, and should have caused, therefore,
hemiopia also, recognizable in the eye on the side of the lesion.*
But the pathological appearances suggested that the disease
of the occipital lobe was later than that of the angular gyrus ;
and such hemiopia might well have escaped detection diuing
the later stages of the patient's illness. The original report
of the case gives no indication that it was sought for.

Hence it is in a high degree probable that (as Ferrier
has suggested) in or near the angular gyrus there exists a
visual centre, higher than the half-vision centre, in which
the whole of the opposite field is represented. For this
relation there must be a connection between this centre on
one side and both occipital lobes, that with the opposite
occipital lobe being probably by means of the fibres of the
corpus callosum. Indeed, the arrangement is probably even
more complex. The crossed amblyopia is accompanied by a
much slighter restriction of the field of the other eye,
i.e.y on the same side as the lesion. Hence, in each higher
visual centre both fields must be represented, that of the
opposite eye, however, far more extensively than that of the
eye on the same side. Another difference may be traced

* I have recorded in "Medical Ophthalmoscopy" (2nd Ed., Case 30, p. 311)
a case in which total blindness of the left eye, with left hemiopia in the
right, accompanied left hemiplegia — all due, no doubt, to an extensive lesion
of the right hemisphore.

K

between tlxis and the half-vision centre. A permanent lesion
of the latter eauaes permanent hemiopia ; hut the crossed
amhlyopia soon lessens, and before long hecomea shght.
This is probably by the substitutionary ad:ion of the centre
of the opposite hemisphere, since in each, as we have seen,
both fields are represented. Ijastly, a lesion of the higher
centre, whatever its exact seat or nature, seems always to
oanse the same form of impairment (amblyopia, restricted
fields, loss of colonr-vision), which differs in degree, but not
in form. A partial lesion seems to lower the function as a
whole — an indication that the function is diffuse,— and this
is probably a characteristic of all the higher cortical centres.

Onr knowledge of the central relations of the olfactorj'
nerve is much less extensive. The only indication affoi-ded
by experiment is that there is a cortical centre for smell at
the anterior extremity of the uncinate gyrus on the inner
surface of the hemisphere (Feirier). Towards this some of
the fibres of the olfactory nerve seem to pass dii-ectly.
Moreover, disease adjacent to these fibres has caused loss of
amel! on the same side as the lesion. On the other hand,
disease involving the "sensory crossway" has impaired
smell on the side opposite to the lesion. Henoe, it seems
pixibable that the olfactory path passes first to a cortical centre
in the same hemisphere, and thence to the other hemisphei"e,
although where it crosses, and what is its idtimate cortical
destination, we do not know, except that the latter is on the
outer surface of the hemisphere. This is shown by the cjise
described on p. 16.

The auditory nerves pass to nuclei situated at the junction
of the pons and medulla oblongata. Theii- exact position we
shall consider presently. They have an extensive connection
with the cerebellum, to which, indeed, some fibres of the
auditory nerves seem to pass directly. You doubtless re-
member that one part of the auditory nerve (from the semi-
cirtmlar canals) has nothing to do with hearing, but conveys
information, as to the position of the body, to the centre

J

SPECIAL SENSE CENTRES. 25

for equiKbration, probably situated in the cerebellum. The
auditory path to the hemispheres probably passes up the pons,
crossing early, and, in the cms, occupies the superior portion
of the tegmentum. Some have thought that it does not pass
up the pons, but passes through the cerebellum ; but this is,
on the whole, improbable. Its course in the cerebrum is
by the "sensory crossway," through the white substance,
to the first temporo-sphenoidal convolution, which all evidence
shows to be the cortical centre for hearing, each centre
receiving impressions from the auditory nerve on the opposite
side.

Of the path of taste, we know only that it passes by the
sensory crossway; of its cortical centre we know nothing.
Strangely enough, even the nerve of taste is still somewhat
uncertain. It is commonly supposed that the glosso-
pharyngeal is the nerve of taste of the back of the tongue,
and that the chorda tympani of the facial, which is certainly
the nerve of taste for the front of the tongue (and probably
comes from the fifth by the Vidian nerve, that passes from the
spheno-palatine ganglion to the facial), may ultimately be
derived also from the glosso-pharyngeal. But I believe that
it will be f oimd that taste-impressions reach the brain solely by
the roots of the fifth nerve, and that the doctrine that the
roots of the glosso-pharyngeal nerve have anything to do
with taste is a curious physiological myth, due to too wide an
induction from certain anatomical facts, and from dubious
experiments on animals. Some time ago* I published a
case in which there was an isolated palsy of one fifth nerve,
motor and sensory portions, due certainly to disease of the
root at the surface of the pons, in which taste was entirely
lost on that side, not only at the front of the tongue, but also
at the back, on the soft palate, and on the palatine arches —
lost to every form of stimulation, whether by sapid substances
or by the voltaic current. The symptoms in this case are
permanent, and I have repeatedly demonstrated the loss to

* ** Journal of Physiology," vol. iii., p. 229.

those who have attended my practice at the Queenoquare

Hospital. Siuee the puhlJcation of that case I have met with
only two other cases in which there was intracrnnial disease of
the fifth without evidence of any interference with the nerves
of the medulla, and in each of these there was the same absolute
loss, at the baek as well as at the front, demonstrable with
ease, and most striking by compariBon with the other side.
It 18 pdssihle that the nerve-fihres for taste on the back of the
tongue may be drRtribufed with the glosso-pharyugeal, reaehing
them from the otic ganglion of the fifth by the small peti-osal
nerve and tjTupanie plexus. This explains the remarkable
fact, pointed out by Urban tschitsch, and which I have several
times observed, that taste may be lost on the back as well as
the front of the tongue, in consequence of caries of the walls
of the tympanum. This course seems, I confess, sti-angely
circuitous, but it is scarcely more circuitous than that which is
certainly taken by the taste-fibres of the front of the tongue.
If this arrangement is ultimately proved beyond question, it
will be of much interest, as bringing the sense of taste into
the functions of one nerve, and that one the nerve that is so
intimately associated with the other special senses of smell,
sight, and heariug.

r

We may conveniently consider next the ari'angement of the
nuclei from which the other cranial ner\-Bs arise. These are
situated in the grey matter that suiTounds the highest part of
the central canal of the spinal cord, the continuation of this
canal between the foiu±h and third ventricles, and that which
lies beneath the floor of tlie fourth ventricle. The nuclei are
colunms of nerve-cells, small in transverse section, but prolonged
in the direction of the axis of the medulla. (See Fig. 10.) The
upper part of the hypoglossal nucleus lies close to the middle
hne in the point of the calamus scriptorius ; lower down it lies
on each side of the middle line in front of the central canal.
In corresiwnding position behind the canal is the column of
cells of the vago-aceeasorial nucleus. In the calamus this lies
mtside the hypoglossal, and gives origin to the pneimiogastric ;
while below, part of the spinal accessory spiings from it. The

J

ORIGIN OF CRANIAL NERVES. 2l

Bpinsl part of the aec^sory consists only of spinal fibres that
rise into a temporary companionship with a higher nerve, but
have the same origin, and subside to the same distribution,
as the other spinal nerves o£ the same level. Note, however,
the proximity of the nuclei of the hypoglossal and accessory
nerves ; both supply muscles that act together in articulation.
Moreover, the muscle that raises the palate and shuts off
the posterior nares in articulation is certainly supplied
from one of the nerves of the medulla, probably from
either the glosso-pharyngeal or the spinal accessory. All

III, third nerve QueleuB ; IV, fourtli ; Vs, middle sensory nucleus of the fifth ;
V m, motor nucleus of fifth ; VI, sixth ; F, facial ; Au, auditory ; H,
hypoglossal ; V a, vago^aecessorial nucleus, the iijiper partgiving origin
to the pneumogaatric, the lower to the highest fibies of the apiual
accessory. Where one iiucleua lies beneath another, its outline is
indicated by a dotted liue.

these three parts — tongue, palate and vocal cord — are para-
lysed together from disease at the surface of the medulla,
damaging the roots of the nerves. All these part« are paralysed

«0 I.KtTURE II.

together in degeneration of these nuclei, with the addition
also of the Kps, constituting the chronic form of " lahio-glosso-
laryngeal paralysis," or " bulbar paralysis." Why the lips ai'e
also affected we shall see pi'esently. The pneiimogaBtric nucleus
in the floor of the ventricle corresponds nearly in position to
the respiratory centre, and no doubt also to the cftrdiac centre.
Its upper and outer limits are not definable, since it blends
with a more difEuse area of delicate grey matter that extends
as far as the auditory nucleus. Outaide, and rather in front of
the upper part of the pneumogaatric nucleus, is the small column
of nerve-eellfi from which the glosso-pharyugeal nerve arisea.

The auditory nucleus is situated at the level of the auditory
striEe, and chiefly in the outer part of the floor of the ventricle,
just overthe commencement of the inferior cerebeUar pedtmcle,
but it extends inwards almost to the middle line. It is a double
nucleus, consisting of inner and outer parts. Fibres are said
to pass from it to the cerebelltma, and some fibres of the nerve
seem to turn aside, and joining those of the restiform body,
pass directly to the cerebellum by its inferior peduncle. The
significance of this connection with the cerebellum has been
already mentioned-

Above the auditory striaa, tmder a prominence on the
eminenfia teres, close to the middle line, is the nucleus of
the sixth nerve. It was once thought to be the comnnm
nucleus of the sixth and facial, — a strange combination, since
these nerves have no functional association. The facial
nerve ascends to this nucleus, forms a loop round it (some
fibres, indeed, go tlirough it), and then passes downwards,
forwards, and outwards, to a column of cells more deeply
placed in the medulla than any other nucleus in the lower
part- A rare case, in which there was total palsy of all
the ocular nerves, and no paralysis of the facial, afforded me
an opportunity of proving beyond doubt tbat the facial nerve
has no real origin from the nucleus of the sixth. All the
cells of this nucleus were degenerated, but the fibres of
the facial were perfectly healthy, and could be traeed
unchanged through the nucleus. The cells of the true
facial nucleus cannot he traced far below the level of the

J

ORIGIN OF CRANIAL NERVES. 29

auditory striee, but it is probable that some fibres of the facial
nerve, those that innervate the orbicularis oris, descend to
the level of the hypoglossal nucleus, and may even arise
frdm this nucleus. The transverse muscle of the tongue and
the orbicularis act together. Neither can contract or relax
without the other. Try, yourselves, gentlemen, when you
are alone with a looking-glass, and you will find that this is
true. Both, moreover, suffer together in degeneration of
the nuclei, while the other parts of the facial nerve escape.

The chief nucleus of the fifth nerve Kes above the sixth,
and at the outer part of the floor of the ventricle. The
fibres of the nerve pass backwards and slightly inwards, and
end in a sensory nucleus on the outer, and the motor nucleus
on the inner side. This is, however, but one part of the
sensory nucleus. Some fibres pass down the medulla, and
can be traced as low as the commencement of the spinal cord.
They have grey matter on their outer side, in which they
probably end. No doubt these fibres bring sensory impres-
sions from the tongue, etc., into relation with the motor
nuclei for these parts. Moreover, the distribution of the fifth
nerve to the skin joins that of the cervical nerves both on the
face a;nd back of the head, and the continuity of the cutaneous
distribution is no doubt subserved by a continuity of the grey
matter, in which the lower root arises, with that from which
the cervical nerves arise. Another group of fibres of the
fifth passes up beneath the corpora quadrigemina, no doubt
subserving the intimate connection between the fifth nerve
and the organ of vision, of which so obtrusive an instance
is presented in the photophobia of conjunctivitis.

The third nerve, entering the inner side of the crus, passes
back to a column of nerve-cells beneath the aqueduct of
Sylvius, not far from the middle line. The combined teaching
of experiment (especially of Hensen and Voelcker) and
of cKnioal observation shows that there are three centres in
this column of nerve-cells, distinct at least in function and
in pathological liability. The most forward of these is the
centre for the ciliary muscle (accommodation) ; the second is
the centre for the light reflex of the iris ; the third, which

LECTURE 11.

occupies the greater part of the nucleiis, ia the centre for the
external muscles supplied by the third nerve.

The fourth nerves differ in two respects from any other
of the cranial nerves. First, they arise above the fourth
ventricle, their origin being from the valve of Vieussens,
hut they curve round the lower part of the aqueduct of
Sylvius to a col umn of nerve-cells that is really the lowest
part of the third nerve nucleus. Secondly, alone of all the
crania) nerves, the fourth nerves decussate between the surface
attachment and the nucleus. But the whole of the fibres do
not come from this nucleus. Some descend the pons, and
probably arise from the nucleus of the sbcth nerve. Indeed,
there seems to be an extensive connection, by large nen'e-

£_a 4

P

C Q, corpora qiiadrigemiiia ; 3, third nerve i III, its nuclous ; i, fourth nerve ;
IV, itsnnelBus, the poaterior part of the third ;6, sixth nerve. The pro-
hable poflitiou of the Mntra and nerve-fibres foi' accommodation ia ahown at
a and a'; for tha refles action of iris at 6 and b' ; for the external muflclea
at c and c*. Tiie lines lieDeatb tho Boor of the fourtll ventnrle indicate
the fibres that connect the nuclei.

fibres, the "posterior horizontal fibres," between the three
nuclei for the nerves of the external ocular muscles (Plechaig),
It is possible that some of these are fibres of the nerves
which reaUy pass by their proper nucleus, and arise from
one of the other nuclei, and the visible decussation of the
fibres of the fourth ner\'e may be the indication of an
extensive decussation of these connecting fibres. Thus we
can understand how the apparently simple arrangement of
the nuclei, and their apparently strange separation in three
distmct groups of nerve-cells, may cover an extensive and

J

ORIGIN OF CRANIAL NERVES. 31

complex structural association, whereby one nucleus may
give origin to fibres that run in several nerves, and the various
nuclei may be blended into what is practically a series of
centres very different from their apparent form. Thus, too,
we can imderstand how these nuclei may govern the complex
movements of the eyes, in which many muscles of both sides
act together in the most perfect synchronism and exact
gradation of effect.

The third, sixth, and hypoglossal nerves arise at the surface,
near the middle line, and pass back to their nuclei between
the middle line and the motor pyramidal tracts. The spinal
accessory, pneumogastric, glosso - pharyngeal, and facial
nerves arise on the surface at the outer part of the medulla,
on the outer side of the pyramidal tracts, and pass inwards
and backwards to their nuclei. The nuclei of the auditory
nerve lie almost immediately above its origin, and one part
of the nerve passes directly back to it, while the other curves
round and above the outer nucleus to reach the inner nucleus.

From all these nuclei, paths, as yet only partially traced,
ascend to the cerebral hemisphere. They certainly cross the
middle line not far above the nuclei. The paths, motor and
sensory, probably join, or at least run close to, the motor and
sensory paths from the limbs. This, as we have seen, is
certainly the case with the motor path of the face.

After leaving the brain, the nerves have a short course
before entering the dura mater. Most arise in the pos-
terior fossa. The nerves to the orbit and the fifth nerve leave
the skidl in the middle fossa, but as they leave the posterior
fossa they pass into the dura mater. Remember that the sixth
nerve has by far the longest course before it enters the dura
mater, from the posterior border of the pons to near its anterior
border, and that before it enters the wall of the cavernous
sinus it passes very near the fifth nerve. Remember also that
in its course over the convexity of the pons it readily suffers
from pressure, if there is any cause of pressure beneath the
tentorium. For this reason, paralysis of both sixth nerves is
a very common symptom in disease of this region.

LECTUEE III.

MEDICAL ANATOMY OF THE BRAIN (Continued) : CONNECTION
OF CEREBRUM AND CEREBELLUM — BASAL GANGLIA-
CEREBELLUM— BLOOD-VESSELS OF THE BRAIN.

Gentlemen, — ^We must now return to some points that
we passed over in considering the anatomy of the cerebrum.
What is the course of the fibres that constitute the anterior
limb of the internal capsule, lying between the body of the
caudate nucleus and the lenticular nucleus ? They pass, on
the one hand, to the cortex of the prefrontal lobe, i,e.y the
frontal lobe in front of the ascending frontal convolution.
On the other hand, they descend into the cms, and occupy
the inner (medial) portion of the crusta, lying to the medial
side of the pyramidal tract. They descend to the pons, and
there seem to end in the grey matter which is so abundantly
scattered among the white fibres, longitudinal and transverse,
of the anterior region of the pons. It is, however, probable
that other fibres, proceeding from this grey matter to the
cerebellum, continue the path to the cerebellar hemisphere,
especially to the lateral and posterior regions. Thus this
tract consists of fronto-cerebellar fibres. They degenerate
downwards, and therefore probably conduct downwards ; but
this degeneration only extends to the pons, being arrested, as
secondary degeneration always is, by the grey matter that
interrupts their course. When the cerebellum is congenitally

CERBKKO-CEBEBELLAR FIBRES.

absent theee fibres are also absent {Fleebsig) . It is probable
that this cx)imeotion is a crossed one, the frontal lobe on one
side being connected with the cerebellar hemisphere of the
opposite side.

FlO. 12. — DlAGRAUMATIC HO&IZOHTAL SECTION, THROUGH THE CGRBBRVK,

Pons, and offosite Hemispberf. of the Cbhebelluu, to show the
couhsb op the fibre8 connectino the frontal and occipital

Lobes with the Cbbebbllpm.
In the section of the crus, on tlie left side, T C shown the position of the
fibrBB to the teLiporo-occipital lobe froDi the cerebellum (shown by
dotted lilies], and F C thnt of the fibres bom the frontal lobe to the cere-
bellum (shown by broken lines) that occupy the anterior limb of the
internal capsule. The other letters are explained on p. 12.

I told you that the outer fibres of the crusta of the crus
oerebri, the fibres that he outside those oi the pyramidal
tract, do not pass up into the internal capsule, but radiat« into
the occipital and temporal lobes of the brain, passing from the

h

34 LF.CTITHE IIT.

cru8, partly beneath the posterior extremity of f
nucleus, partly between it and the external corpus genicu-
latum. These fibres connect these lobes with the cerebellum
in the same way as the fibres of the inner part of the eras
connect the frontal lobe with the eerebellnm. Their connection
is chiefly with the upper siirfaee of the cerebellum, near the
middle lobe, and it is probably also crossed. These fibres do
not degenerate downwards, and therefore probably conduct
upwards. They are also absent when there is no cerebellum.
The small bundles of fibres that lie behind, or rather above,
the pyramidal tract in the cnista, between it and the sub-
stantia nigra (Fig. 5), consist of fibres that descend from the
corpus stiiatiun, caudate nucleus, and outer part of the
lenticular nucleus, and, reaching the pons, probably connect
those parts with the cerebellum in the same way as the
other tracts connect with it the cortex.

This extensiye oonneotion of the cortex with the henu-
ispheres of the cerebellum ia a fact of extreme interest, beoause
the parts of the convolutions thus connected are those in which
there is the least definite locahzatiou of motor and sensory
function. In the prefrontal lobe of the human brain there is
at present no evidence of motor function. In the temporal
lobe we have only the auditory centre in the first convolution.
In the occipital lobe we have only the ^-isual centre, which,
although not yet accurately defined, probably occupies only a
part, of it. In these portions of the brain a lesion may exist,
and cause neither motor nor sensory sjinptoms ; their function
is more diffuse, so to speak, and thus capable of supplementary
substitution. It is here that we must look for the processes
oonceraed in the higher inteUectual operations. These parts,
whatever other connection they may have, seem to be con-
nected with each other through the cerebellar hemispliere by
the downward path from the frontal and the upward path
to the temporal and occipital lobes. This very curious fact
revives the old idea, that the cerebellum is, in some way,
concerned in intellectual processes — an idea suggested by the
proportion that the cerebellar hemispheres bear to intellect
as we ascend the scale of animals. Moreover, the oerehellar

J

BASAL GANGLIA. 35

hemisphere has this in common with the parts of the cerebral
cortex with which it is connected, that a lesion may exist
in it without motor or sensory symptoms.

You may have observed with surprise that I have said
nothing about the great central ganglia of the brain, which
were formerly supposed to have such important connections
with the motor and sensory tracts. It is probable that some
of them have a connection with motor centres, but it is
certain that their relations are very different in nature from
those formerly attributed to them.

The optic thalamus receives fibres from below that come
from the tegmentimi of the cms, and probably these are
derived from the upward sensory path from, the spinal cord.
It also receives fibres from the superior peduncle of the
cerebellum; perhaps also from the optic nerves. From it
fibres radiate to all parts of the cerebral cortex. Some go
to the lenticular nucleus ; but we do not know whether they
end in it, or pass through it to the convolutions. Never-
theless, it does not seem to be in the path of those common
sensations that affect consciousness. These pass, as we have
seen, outside the hinder part of the thalamus, in the posterior
third of the internal capsule. They are close to the thalamus,
its lesions often involve them, but when they are imaffected
there is no loss of sensation. It is highly probable, however,
that the thalamus is concerned with some of the higher
reflex processes.

The grey masses of the corpus striatum, on the other
hand, seem to have no connection with the cortex. The
caudate nucleus is connected with the cerebellum, as we
have seen, by fibres that enter the internal capsule, either
directly, or after passing through the lenticular nucleus,
and lie in the cms close to the locus niger, reaching the
cerebellum by the middle peduncles, after interruption by
grey matter in the pons. No fibres from the caudate nucleus
seem to join the pyramidal motor path. The lenticular
nucleus, like the optic thalamus, receives fibres (chiefly

D 2

LKCTliKE III.

collected into the "lenticular loop") from the tegmentum
and from the oppoaite superior cerebellar peduncle. Thus
both porta of the corpus striatum have an extensive con-
nection with the cerebellum of the opposite side, and the
descending fibres from the caudate nucleus degenerate (and
therefore conduct) downwards, while those from the cere-
bellum to the lenticular nucleus probably conduct up-
wards. Thus tluB connection presents considerable analogy
to that between the cortex and the cerebellum. In con-
genital absence of the cerebellum the corpus striatum is
reduced to a third of its ordinary size (Plechsig). It seems
prohable that the two parts of the corpus striatum are central
organs, analogous to the cortex itself. The analogy to those
parts of the cortex that are connected with the cerebellum
is rendered etiU greater by the fact that a lesion, even an
extensive lesion, may exist in either the caudate or lenti-
cular nucleus, and so long as it does not interfere with the
functions of the motor or sensory parts of the internal capsule,
it causes no symptoms.

Although the middle lobe of the cerebellum is continuous
Avith the hemispheres, and the peculiar foliated cortex has
a similar structure in both parts, it is certain that there is
an essential difference in their function. In the white
substance of the middle lobe are several curious nuclei of
grey matter. As we dracend the scale of animals the
hemispheres become smaller, until the cerebellum, of birds
for instance, corresponds only to the middle lobe. The
hemispheres may be diseased without recognizable symp-
toms, but this is not true of the middle lobe. The disease
of this causes the peculiar unsteadiness of movement long
known to be characteristic of cerehellar disease, and lately
shown (by Nothnagel} to be characteristic only of disease
of the middle lobe. The reason why the latency of lesions
in the hemispheres was so long imrecognized is because the
common lesion is tumour, and this almost always presses
on the middle lobe. We must thus regard the middle lobe
of the cerebellum as in some way concerned with the main-

CEREBELLUM OLIVARY BODIES — VESSELS. 37

tenance of equilibrium, perhaps by combining the afferent im-
pressions, and arranging for harmonious centrifugal impulses.
This view is supported not only by the effects of disease, but
by the facts that certainly towards this lobe, and probably to
it, fibres pass from the posterior columns of the cord, from
the direct cerebellar tract (fibres from the lower trunk-
muscles), and from the auditory nerve. Ferrier foimd that
stimulation of the middle lobe caused movements of the
eyes. Although we cannot conceive that centres for the
voluntary movements of the eyes exist here, yet the eye-
ball muscles furnish important guidance to the centre that
regulates the maintenance of equilibrium, and the centre
for these muscles may thus be so related to the central lobe
of the cerebellum, that its stimulation may cause indirectly
the contraction of these muscles.

No part of the brain has excited more interest and re-
ceived more study than the olivary bodies of the medulla ;
varied fimctions have been, in turn, ascribed them, but these
hypotheses, destitute of foundation, have successively sunk
out of view, and we are still ignorant of the function of
these structures. Their connections are peculiar. The
bodies resemble closely the dentate nuclei of the cerebellum ;
aad the resemblance is certainly not accidental, for the two
structures are connected by fibres, and atrophy together.
Each olivary body receives fibres from the posterior columns
of the cord on the opposite side, and is connected with the
dentate nucleus, also of the opposite side. From each dentate
nucleus fibres pass to the superior cerebellar pedimcle and
tegmentimi of the opposite crus. Thus the tegmentum of
one crus cerebri may be connected with the olivary body of
the same side through the opposite dentate nucleus.

A large nimiber of cerebral lesions are produced by
disease of the cerebral vessels, by their occlusion or their
rupture. To imderstand many facts about these lesions, you
must know the arrangement of the cerebral vessels and the

LECTURE III.

conditions of tie cerebral circulation. I will briefly mention
to you the facta of chief importance. Those that concern the
arterial system have been ascertained by the investigations of
Duret in France, and Heubner in Germany.

The blood-supply to the brain comes from the carotid and
vertebral arteries. The left carotid arises from the aorta nearly i

in the direction of the current of blood that courses through
the aortic arch ; while the right carotid comes fi'om the
innominate, and this arises from the aorta nearly at right
angles to the current of blood. Hence solid particles are
rather more readily carried into the left than into the right
carotid — a circumstance that explains the somewhat greater
frequency of embolism on the left side of the brain. There
is a similar but still greater difference in the origin of the
two veitebrals, and it is probably for this reason that the left
vertebral is often larger than the right. This does not
determine any difference in the frequency of vascular lesions
in the part of the cerebrum suppHed, because the blood
brought by both vertebrals has to pass through the common
basilar. The internal carotid, on each side, divides into a
small anterior cerebral, and larger middle cerebral. The
latter continues the dii'ection of the internal carotid, and
hence plugs carried from the heart readily pass into it.
The " circle of Willis," you will remember, is formed by these
vessels, together with the anterior communicating artery,
between the anterior cerebrals, and two posterior commuoi-
cafing (one on each side), between the middle and posterior
cerebrals.

From the circle of Willis and the commencement of the
three cerebral arteries (anterior, middle, and posterior) small
branches arise which supply the central ganglia and adjacent
white substance of the hemisphere, while the three arteries
ramify over the surface of the brain, and supply the grey
cortex and the chief part of the white substance. Thus there
are two systems of branches, central and cortical. Between
these two systems there are no anastomoses. The central
branches do not communicate with each other, and hence
^ obstruction of one causes necrosis of the region supplied, no

P J

CEREBRAL CIRCULATION. 39

collateral supply of blood being possible. The cortical
branches vary in this respect in different individuals. In
some persons there is enough communication between the
cortical branches to maintain nutrition if one is obstructed ;
in other persons there is no communication. Hence obstruc-
tion of the middle cerebral at its origin always causes necrotic
softening of the part of the central ganglia that it supplies,
and sometimes also softening of the cortex ; while in other
cases, with a similar obstruction, we may find that the cortex is
intact, although the central ganglia are extensively damaged.
The branches to the ganglia must engage our attention
in further detail, since the pathological importance of these
"central arteries" is very great. They are divided into
six groups, of which two are medial and small, and four
(two on each side) are lateral' and very important. The
anterior medial group is given off by the anterior cerebrals
and anterior communicating artery, and supply the anterior
extremity of the caudate nucleus. The posterior medial
group consists of twigs given off by the posterior cerebrals
near their origin. Passing through the posterior perforated
spot, they supply the inner part of the optic thalamus and
the walls of the third ventricle. These two medial groups are
insignificant in the extent of the brain supplied by them, but
of some pathological importance, since haemorrhage, from
their rupture, is apt to burst into the ventricles. The lateral
groups furnish the blood to the chief part of the central ganglia
and the internal capsule. The anterior lateral group consists of
numerous small arteries that arise from the middle cerebral
in the first inch of its course, pass through the anterior
perforated space, and supply the caudate nucleus (except its
head) , the lenticular nucleus, internal capsule, and part of the
optic thalamus. Some pass through the inner part of the
lenticular nucleus to the internal capsule ; while others pass
first outside the lenticular nucleus, and then through its outer
portion to the capsule. They supply the caudate nucleus and
optic thalamus after passing through the capsule. These
vessels are prone to rupture, perhaps because their direct
origin from a comparatively large vessel exposes them to

a high hlood-presBure. Hence the frequency of cerehral
heemorrhage in this situation. The arteries of the posterior
lateral group arise from the posterior cerebral, and supply
the hinder part of the optic thalamus. Htemorrhage from
their rupture usually damages the posterior (sensory) part
of the capsule, and often extends into the cnis. Branches
from the posterior cerehral supply also the cms and corpora
quadrigentina.

Of the blood-supply to the corffix, that from the middle
cerehral is both the most extensive and the most important,
embracing, as it does, the central (motor) convolutions. The
general arrangement of the branches of each artery is the
same : each divides and ramifies, and from the branches, and the
ultimate ramifications in the pia mater, twigs are given off to
the cerebral substance — some short, that end in the grey cortex ;
others long, that pass through the grey cortex to the white
substance, extending in it to various depths. The regions
supplied by the several vessels are as follows : — The anterior
cerebral, curving roimd the corpus eallosum, suppUes, by three
branches, part of the orbital lobule, and the inner surface of the
hemisphere as far as the quadrate lobule (precuneus). It also
Bupphes, on the outer surface, by branches that come over from
the inner surface, the first and second frontal convolutions,
and the highest part of the ascending frontal. The middle
cerebral or " Sylvian artery " divides in the fissure of Sylvius,
opposite the island of Eeil, into four branches, which He in
the sulci of the insula, and then pass — the first to the inferior
frontal convolution ; the second to the ascending frontal,
except the highest part, which is suppHed by the anterior
cerebral ; the third to the whole of the ascending parietal, and
the adjacent part of the inferior parietal lobule ; the fourth
to the convolutions about the posterior limb of the fissure of
Sylvius, supramarginal and angular, the hinder part of the
superior parietal lobule, and the first temporal. From this
vessel, near its origin, one or two large branches arise that
supply the greater part of the second and third temporal con-
volutions. The posterior cerebral suppHes the occipital lobe,
and also the inferior aspect of the temporal lobe, by three

CEREBRAL CIRCULATION. 41

brandies, of which one goes to the lower part of the uncinate
convolution, a second to the inferior part of the temporal lobe,
and a third to the cuneus, lingual convolution, and the inner
and outer surfaces of the occipital lobe.

Thus the middle cerebral supplies the motor region, both
central and cortical, except in part the leg-centre ; it also
supplies the part of the cortex that subserves cutaneous
sensibility, the cortical auditory centre, and probably the
higher visual centre ; it supplies all the cortical regions
concerned in speech-processes in the left hemisphere, motor,
auditory, and visual. The anterior cerebral supplies only a
small part of the motor region, viz., the part of the leg-centre
that occupies the paracentral lobule and highest part of the
ascending frontal. The posterior cerebral supplies the visual
path, from the middle of the tract backwards, and the half-
vision centre in the occipital lobe ; it supplies also the
corpora quadrigemina, and the sensory part of the internal
capsule.

The pons and meduUa receive small arteries from all the
adjacent vessels, vertebrals, basilar, and cerebellar arteries.
These branches are in two sets — ^median, near the middle line ;
and lateral or radicular, that pass in at the side, near the chief
nerve-roots. Both pass back to the nuclei near the floor of
the fourth ventricle, but the chief blood-supply to these nuclei
comes from the median branches. Of the cerebellar arteries,
the superior and inferior supply the corresponding regions of
each hemisphere, and the upper surface is also supplied by
a large branch from the basilar opposite the middle of the
pons, the middle cerebellar artery. These arteries com-
municate freely, and hence necrotic softening of the cere-
bellimi is rare. The branches to the medulla and pons do not
communicate, and hence here necrotic softening is common.

The venous circulation of the brain presents several im-
portant peculiarities. The veins from the greater part of the
cortex pass upwards to the longitudinal sinus, and open into
this in a forward direction. This arrangement involves two
very unusual conditions. Elsewhere, the blood from ascend-

ing arteries paasea into deaoending veins, bo that the feetle
preesure that passes tlirough the capillaries is supplemented by
the influence of gravitation. Elsewhere, ascending veins convey
blood that has been brought by descending arteries, and the
venous flow is aided by the hquid pressure, which, according to
the well-known law of hydrostatics, tends to make the blood
rise in the veins. Bnt on the brain, the blood from asoending
arteries passes into ascending veins. The openings of these
veins into the longitudinal sinus being directed forwards, the
entering blood is opposed in direction to the current in the
sinus, and the effect must be to retard the flow in both veins
and sinus. Moreover, in the erect posture the anterior half of
the longitudinal sinus has also an ascending course, while the
trabeculffi that occupy the lumen of the sinus must offer some
hindrauoe to the movement of the blood. These circum-
stances help ua to understand the readiness with which clots
form in the cortical veins and longitudinal sinus, when
other eireumstanoes favour the coagulation of the blood.
Indeed, the marvel is that thrombosis is not more common
than it is.

The veins of Galen, conveying blood from the ventricles
to the straight sinus, pass above the corpora quadrigemina
and middle lobe of the cerebelhun, and are readily com-
pressed by tumours in this situation. The course of the
veins at the base is not of much medical importance.
The blood from the internal ear passes into the cavernous
sinus, that from the mastoid cells into the lateral sinus ; and
septic clots may thus extend when there is caries of the
temporal bone. Many sinuses receive veins from the diploe
of the skull.

There is very Kttle communication between the individual
veins of the surface, and hence obstruction of one causes
grave damage to the cerebral tissue. The sinuses, however,
communicate freely, and there are certain communications
between the intracranial veins and those outside the sktill.
The veins of the nose communicate with the anterior ex-
tremity of the superior longitudinal sinus, and hence epistaxia
relieves venous congestion within the skull. The ophthalmio

CEREBRAL CIRCULATION. 43

vein (going to the cavernous sinus) communicates with the
facial, and hence pressure on the sinus causes little or no
distension of the retinal veins, because the pressure is quickly
relieved. The mastoid veins effect a communication between
the lateral sinus and the occipital veins. Moreover, many
emissary veins pass through small foramina in the skull, and
connect certain sinuses with external veins, the most im-
portant being between the longitudinal sinus and the veins of
the scalp, and the inferior petrosal sinus and the deep veins
in the neck. A further communication, variable in degree,
is effected by the veins of the diploe. These communications
are important, because they explain, first, the extension of
morbid processes from the exterior to the interior of the
skull, and secondly, the occasional occurrence of external
tumefaction when intracranial sinuses are obstructed by
thrombosis.

LECTUEE IV.

SYMPTOMS OF BRAIN DISEASE: MECHANISM OF THEIR PRO-
DUCTION— MOTOR PARALYSIS— HEMIPLEGIA.

Gentlemen, — ^Tou may remember that in describing to you
the principles of the diagnosis of diseases of the spinal cord, I
insisted on the importance of keeping not only distinct, but
separate in your mind, the two parts of the diagnosis — ^the
seat of the disease and the nature of the disease — ^the former
indicated by the sjonptoms present, the latter by the mode in
which they came on. The distinction is equally important in
the diagnosis of diseases of the brain ; but the separation is
not equally practicable. The sjonptoms themselves are in-
fluenced by the nature of the disease to a far greater extent
than in the case of diseases of the spinal cord. After we
have ascertained the seat of the disease, we have to determine
its nature, and then to consider how far the symptoms
present are further explained by the character of the lesion.
It is convenient to follow the method adopted in the case of
diseases of the spinal cord, and, having considered in the last
lecture the most important facts at present ascertained re-
garding the structure and functions of the brain, to study
next the symptoms produced by its diseases, and afterwards
the relation of these symptoms to the seat and nature of the
morbid change.

Before we study the several symptoms, it is well to know the
various mechanisms by which they are produced — ^mechanisms

SYMPTOMS MEGHAN ISM. 45

common to many morbid processes. The first of these is
by the destruction of cerebral tissue. The function of the
part destroyed is necessarily lost, and the loss is permanent
imless it can be compensated by the action of some other part
of the brain. In some parts of the brain the function is, as
I have said, diffuse, and extensive compensation may occur.
Although a loss of tissue, however small, doubtless has its
effect, the evidence of the loss may be scarcely appreciable
unless the lesion is extensive. When the loss does occur, it
is manifested rather by a general lowering of function than
by any special loss. This is the case with those regions
of the brain that are probably concerned with the higher
intellectual processes, as the prefrontal lobe. Some other
functions are performed only by certain structures, and if these
are destroyed, that function is permanently lost. Between
these two groups there is another, in which special functions
may not be permanently lost, even when the part of the brain
subserving them is destroyed, because these functions are so
related to both hemispheres that the corresponding part of the
imaffected hemisphere can supplement that which is destroyed,
and act for it. If, however, this second centre is also
destroyed, the function is entirely and permanently lost.

Secondly, sjmaptoms may depend on loss of function due to
damage that falls short of destruction. The chief mechanisms
of this damage are compression and defective supply of
arterial blood. In compression both these mechanisms are
combined; the pressure necessarily interferes with the flow of
blood through the capillaries, and causes anaemia. Hence we
do not know how far compression acts mechanically on the
nerve-elements, and how far it acts by narrowing the vessels.
A moderate compression of a nerve soon arrests conduction
through it. If you compress your ulnar nerve behind the
elbow, you soon cease to feel in the fingers supplied by it ; but
even here the compression must render the nerve anaemic,
and we cannot infer that the effect on the fibres is simply
mechanical. In the brain there is a curious fact regarding
pressure which you should remember. Pressure is very much
more effective when it is suddenly produced than when it is

LECTURE IV.

h

slowly produced. The pressure of a cerebral hajniorrhage
causes syraptoms (that we eau certainly refer fo the pressure)
of much greater intensity than does a tumour, although the
latter may be of larger size. It is easier to explain this
difference if we assume that pressure acts mechanically than
if we suppose that it only causes sjTnptoms by producing
amemia.

A diminished supply of ai-terial blood also causes loss of
function. If the supply is altogether cut off, the loss of func-
tion is immediate and absolute. This is true of nerve-tibrea
as well as of nerve-cells. For a short time, perhaps a day,
function may return if the blood-supply is restored ; afterwards
structural disintegration occm-s, and the nerve-elements perish.
Remember that arterial blood may be deficient when there is
no absolute diminution in the amount of blood in the part.
If there is a hindrance to the return of blood by the veins,
the OTer-fiUed vessels cannot receive blood from the arteries,
and so the symptoms of mechanical congestion are to a large
extent the some as those of anteniia.

The nerve- elements may be damaged or destroyed by more
minute morbid processes, either beginning in tlie interstitial
tissue or in the nerve- elements themselves, such as the various
processes of inflammation and degeneration.

The second disturbance of fimction that results from brain-
disease is that which we call "irritation." Irritation causes
two effects. First, there may be a morbid increase of activity
instead of a diminution ; there is evidence of an excessive,
although abnormal, liberation of energy. This disturbance
may be sudden and paroxysmal, or persistent. The former
is often spoken of as " discharge," by an obvious metaphor,
which is, indeed, more than a metaphor. Discharge implies
a preceding charge. The nei-ve-energy liberated in the dis-
charge must have been ready for Hberation, but restrained-
It must have been in a state of " tension" — " held," that is to
say. But " held " by what resistance ? We do not know.
Nevertheless, the fact of a resistance and restraint, co-
extensive with the production of nerve-force, helps us much
in understanding the phenomena of nerve-action in both healtli

SYMPTOMS MECHANISM. 47

and disease. It helps us, for instance, to comprehend what
ha^ seemed to some so strange a paradox, the fact that disease
should cause over-activity. If we conceive, as by all analogy
we may, that the restraint is the highest function of nerve-
cells, — that the self-control, and the capacity for being
controlled, are higher functions than liberation of energy, —
we can understand that when, by disease, there is deteriora-
tion of function, one effect of this is excessive activity.
When the brain is suddenly deprived of blood, one effect
often is to cause convulsions : thus the first result of failing
function may be the liberation of energy. No doubt in irri-
tation the same process is operative. At the same time we
must not deny that some influences may directly augment
the energy-producing action of cells, although we have no
means of proving such an augmentation.

These considerations enable us to imderstand something of
another and remarkable fact — the second effect of irritation.
It may not only cause over-activity of nerve-elements, it
may lessen their activity, and even arrest it. This arrest is
an example of what physiologists term " inhibition." It
may be conceived as an increase of the resistance or restraint.
It is remarkable that the same process should sometimes pre-
vent and sometimes permit the liberation of nerve-force, but
instances of this are familiar to physiologists. The same
stimulus, in different degrees, will either arrest or produce
reflex action. In irritation the nerve-tissues directly affected
may be inhibited or discharged, or their irritation may in-
hibit or discharge connected nerve-cells at a distance. It is
probable that the nervous system is full of mechanisms
whereby the action of certain centres is controlled by that of
other centres, and it is probable that the chief mechanism of
this association is control, and that what we call the excitation
of one centre by another may be very often simply a lowering
of control, permitting activity. Thus we can imderstand that
inhibition, as well as excitation, may be a result of the
pathological process that we call irritation.

Almost all organic lesions of the brain involve these two
processes — damage, complete or incomplete, and irritation.

48 LECTURE IV.

Their relative degree varies, aud still more does their relative
duration. In a sudden lesion there is immediate damage
and immediate irritation. The irritation soon passes off,
unless it is maintained by a secondary more chronic process.
The damage that is incomplete also passes away, and with
it the symptoms that it has caused. The damage that is
complete persists, and its symptoms persist. Henee the
symptoms of an acute lesion of the brain are at first far
wider and more severe than correspond to the actual destruc-
tion. The excess due to slighter damage (as by compression)
and to irritation, soon passes away. It has become cus-
tomary (in Germany especially) to distinguish the two classes
as the "direct" and "indirect" symptoms. The terms are
convenient, although they are not exact, since almost aU the
so-called indirect sjrmptoms are, in one sense, the direct effect
of the lesion.

In disease that is gradual in development and com'se, snob
disease as a tumour, slighter damage and irritation are con-
stantly occurring. The symptoms due to these accompany
those due to the destruction by the disease. Hence the
symptoms of such disease are often complex, and far more
extensive than might have been anticipated. You may
now see the meaning of the st-atement I made just now,
that the nature of the lesion has far more influence on
the character of the symptoms in disease of the brain, than
it has in disease of the spinal cord.

The division into direct and indirect symptoms is founded
on the mechanism by which they are produced, and the dis-
tinction, as we have seen, is not merely theoretical, but is
based on the important fact that, in the case of acute lesions,
the indirect symptoms, however obtrusive at the onset, soon
pass away, while the direct symptoms persist. Unless the loss
can be compensated, it persists as hmg as life endures. We
have now to consider another important division of the
symptoms, founded, not on their mechanism, but on their
cham,ot«r. Some symptoms, such as local palsy, are due to,
and indicate, interference with the function of a definite pait
of the brain. These are termed "focal" symptoms, because

u

SYMPTOMS — PARALYSIS. 49

they are due to disease at a given spot. It is not quite in
harmony with the modem sense of " focus," although there is
always a tendency to associate concentration with limitation ;
but the sense is not altogether alien to the original meaning
of " focus," which, you will remember, is that of a fireplace.
Other symptoms, such as loss of consciousness, or delirium,
indicate a widespread interference with the function of the
brain, and are called ^' diffused This distinction, although
important and useful, must not be conceived as absolute.
Few of our distinctions are absolute. Some symptoms may
be diffuse in one case, focal in another, as, for instance, con-
vulsions. Moreover, diffuse processes may cause focal symp-
toms, and vice versa. Both direct and indirect symptoms may
be either focal or diffuse ; but it is much more common for
direct symptoms to be focal than diffuse, and somewhat more
common for indirect symptoms to be diffuse than focal.

In considering in detail the symptoms, irrespective of their
cause, we will not follow a strictly logical order, but will take
first the symptom that is one of the most conmion, which we
know most about, and therefore should be able to understand
best — ^loss of the power of voluntary motion, motor paralysis.
The loss of power may be complete or partial in degree ; both
have always been, and still are, commonly termed " paralyses."
It has of late become fashionable to call the partial loss
" paresis," a term of doubtful value except as a means of
giving a questionable satisfaction to patients, who find com-
fort in the mysterious word, and think well of its donor — at
any rate until the next physician whom they consult assures
them that the disease is " paralysis," and that " paresis " is
only Greek for weakness. But what is altogether unjustifi-
able is to assert that partial loss of power is not paralysis.

Impairment of motor power is due to interference with
the motor centres in the cortex of the brain, or the motor
path from them by the internal capsule, cms, pons, and
pyramids of the medulla, in the course that we have already
traced. Above the pons the two paths are separate, and a

E

lesion in one erus, or one hemisphere, affects only one motor
tract, causing paralysis of the opposite half of the body —
" hemiplegia," In the pons the two paths are near together ;
both may be affected by a single lesion, and yet they are far
enough apart for one to be often affected alone. In the
anterior pyramids of the medulla they are so near that both
often suffer. A lesion here, on one aide, affect* the arm and
leg on the opposite side. Above the medulla the path from
the hypoglossal nucleus, ha\-ing crossed the middle hne just
above the nucleus, is associated with the tract for the limbs,
and so the tongue is paralysed on the same side as the limbs.
Above the middle of the pons the facial patli joins that of the
limbs, and the hemiplegia involves the face. Thus affection
of face, tongue, arm, and leg on the same side is the charac-
teristic of complete hemiplegia that results from disease any-
where between the cortex and the middle of the pons. The
fibres of the motor path spread out in passiug from the erus
into the internal capsule, and still more widely in passing
through the white substance to the cortex (see Fig. 5, p. 12),
the tracts for tongue, face, arm, and leg being to a consider-
able extent separate, and the separation being greatest at the
cortex. Hence, a lesion, even of some size, in the cortex, or in
the white subatanee beneath the cortex, may affect only one or
two of these parts, the others escaping. The arm, for instance,
is often thus paralysed alone. But even a small lesion of the
internal capsule usually affects all the tracts ; it must be very
small indeed to damage only one of them. If the lesion is
in the erus, although it is very small, all are involved.
Theoretically, it is true, a lesion in the cms or pons may be
BO small as to damage only one part ; but praotieally this is
aearcely ever met with.

The hemiplegia is always on the side opposite to the
cerebral lesion. A few eases have been recorded in which
the hemiplegia was on the same side as the lesion, and these
havS exercised very much the minds of pathologists. But
a much more frequent event is to meet with hemiplegia
without any discoverable lesion in either hemisphere. Some
morbid change must exist in such cases ; and a similar un-

P J

HEMIPLEGIA. 51

discovered lesion in the hemisphere opposite to the paralysis
is the most probable explanation of the cases in which the
only discovered lesion is on the same side as the hemiplegia.
Coexistence does not necessarily involve causation.*

In a case of severe hemiplegia — -" complete hemiplegia," as
it is called — ^the paralysis affects one side, but not the whole of
one side. The arm and leg are powerless ; the face is paralysed
chiefly in the lower part ; the upper part of the face moves
almost as well as on the unparalysed side. The tongue, when
protruded, deviates towards the paralysed side (being pushed
over by the opposite unopposed genio-glossus) ; but the muscles
of mastication contract equally, or almost equally, in ordinary
action, and the two sides of the thorax move equally in
ordinary breathing, or if there is an inequality it passes away
in a few days. But if the patient makes a strong effort,
the masseter on the paralysed side does not contract quite so
strongly as the other, and if he takes a deep breath, and
brings into action the extraordinary muscles of respiration,
there is a distinct defect of expansion of the corresponding
half of the thorax. I remember when I was a student,
learning from two distinguished physicians — from one that
the masseters and respiratory muscles are always weakened
in hemiplegia ; from the other, that they never are. Both
were right, or nearly right. The one had observed only
ordinary movements, the other extraordinary movements.
Other muscles of the trunk are also weakened — ^those; for
instance, of the back and of the abdomen, — ^but the degree
of weakness is always sKght.

Thus some muscles are completely paralysed, some are
merely weakened, others are usually not paralysed at all,
and are never paralysed much. Moreover, this does not
depend on the extent of the disease in the brain. It occurs
when the whole of one motor tract is destroyed. This is
best explained by an hypothesis, first suggested (in a slightly

* The hypothesis of Morgagni, that there is no decussation on the medulla
in these cases, docs not receive so much support as might seem from the dis-
covery of the variability of this decussation, because it is certain that the
medullary decussation, when deficient, is supplemented in the spinal cord.

E 2

LECTURE IV.

difEerent form) by Broadhent. Some muscles are liabitually
used without their fellows on the other side— as the muscles
of one arm. Others are often used with their fellows, hut
often also alone, as the muscles of extraordinary respiration.
Others are never used without their fellows, as the iutercostals,
the frontales, and the masaeters. The degree of paralysis in
hemiplegia ooiresponds roughly to the degree of unilateral
use. The muscles of bilateral use are represented in both
hemispheres of the brain, and the degree of bilateral repre-
sentation oorresponds to the degree of bilateral use. It may
be that the representation of these muscles is ratlier greater
in the opposite hemisphere thau in the hemisphere of the
same side, or that the nervous aiTangements are in greater
functional activity in the opposite hemisphere. Hence there
is sometimes slight weainesa for a short time after the onset
of hemiplegia ; but the hemisphere of the same side is soon
able to innervate them iu full degree. It is possible, although
not yet proved, that the innervation is affected by pyramidal
fibres that do not decussate.

I have said that tliough muscles of bilateral use may he at
first weakened, the weakness soon passes off. In muscles that
are of partial bilateral use the weakness also lessens, although
less quickly. The legs are used much together, although
capable of unilateral use, and the loss of power in the leg
never remains absolute, although it may .remain absolute in
the arm. As a rule, however extensive the lesion, the patient
regains ultimately some power in the leg, and commonly
enough power to enable him to stand. When hemiplegia
occurs in early life, the leg always recovers, and becomes as
strong as the other, even when its growth is retarded. Since
this occurs when the lesion involves the whole of the motor
tract of one hemisphere, it must be through the unaffected
hemisphere gaining by use that power over the leg of the
same side for . which, doubtless, etmctural arrangements
always exist, although they are not called into complete
functional activity under normal conditions.

Another effct follows from this double representation of
the leg. The lesion of the brain causes at first some weakness

HEMIPLEGIA. 53

of the leg on the same side as well as on the other, but
this soon passes off. Doubtless, if we could measure their
strength, the other bilateral muscles would exhibit the same
bilateral weakness.

These phenomena present also another aspect. Most of
these bilateral movements are automatic — ^need little or no
voluntary effort. Movements are lost in proportion as they
require will; persist in proportion as they are automatic.
Again, emotional movements are automatic : the will is needed
not to cause, but to restrain them. Emotional movement
may be preserved when voluntary movement of the same
muscle is lost. For instance, if the patient tries to show his
teeth, the mouth may be motionless on the paralysed side,
and yet if he smiles there may be little or no difference
between the two sides. Emotional movements are probably
innervated from either hemisphere.

Certain movements are normally effected by non-corre-
sponding muscles of the two sides. Such, for instance, are the
lateral movement of the eyes, and the rotation of the head.
In the latter the head is turned to one side by some muscles
of that side acting with the stemo-mastoid of the other. In
hemiplegia these movements are affected, but chiefly during
the early stage. It is the movement towards the paralysed side
that is lost, and the unopposed antagonists may even cause a
slight deviation of the head and eyes towards the unaffected
side, i,€,y towards the side of the brain diseased — ^this is termed
" conjugate deviation." It shows us very clearly that move-
ments rather than muscles are represented in the brain.
The fact that the conjugate deviation occurs, and that it
passes away, shows us two things. It proves, first, that these
movements, though effected by muscles of both sides, are
habitually innervated from the opposite hemisphere, ^.e., the
head is turned to the right by the left hemisphere of the
brain. Secondly, it shows that the movements are also
represented in the hemisphere of the same side, by nervous
arrangements that may readily be called into effective use. .

If a patient is unconscious, we can no longer call his will
into action, and are thus deprived of the direct evidence of loss

LECTVRE IV.

of volTmtary power. If the patient is restless, the absence of
movement on one side may be ohBerved ; and a pinch of the
skin may cause a movement on one side only. There may
also be flacddity of the muscles of the paralysed side, and the
limbs, when raised, fall more suddenly than on the unaffected
side ; or, on the other hand, they may present a distiactlj'
abnormal rigidity. The conjugate deviation of the head and
eyes, if present, aJao indicates a one-sided loss. Moreover,
we may sometimes obtain help by observing the state of I'eflex
action.

It is very common, although not invariable, for the reflex
action from the skin to be lessened or abolished on the
paralysed side. The loss may be observed in the plantar,
cremasteric, and abdominal reflexes. It exists from the
onset. Why this symptom exists in some cases and not in
all, we do not yet know.

The myotatie irritability, evidenced by the so-called
"tendon-reflexes," is often imchanged during the fu-at week,
and at the end of that time becomes excessive, so that the foot-
clonus can be obtained. Sometimes, however, a clonus can
be obtained a day or two after the onset, and there may be,
immediately after the onset, complete loss of these reactions,
ao that even the knee-jerk cannot be obtained. The early
change is to he ascribed to an influence exerted by the lesion
on the spinal centres ; the later increase to the secondary
■ degenerative changes in the pyramidal tracts reaching these
centres.'

At some period the muscles of the paralysed limbs become
rigid, stiffening the Kmbs in certain postures, and opposing
passive movement, Todd fii^ distingiushed between "early"
and " late " rigidity. The former comes on a few days after
the onset, and lasts for a few weeks. The posture of the
limbs is that of rest. It is probably due to the irritation of
the fibres by inflammatory changes about the lesion. But
there is sometimes an " initial rigiditj'," which developes
immediately, and lasts for a few hours or for a day or two. |

• See " Dia^osis nf Diseases of the Spinal Cord," driJ Ed., p. 28, for afuUar ''

dlBCUssion of tliia subject. .

I ^

HEMIPLEGIA. 65

It is probably due to the irritation of the fibres by the lesion
itself. When these forms of rigidity are considerable in
degree we can often obtain the foot-clonus. The rigidity is
the result of that state of the muscle-reflex centres in which
myotatic irritability is increased. Late rigidity comes on in the
course of a few weeks, and persists as long as the palsy. The
shoulder is adducted, the elbow flexed, the wrist pronated and
sKghtly flexed; the fingers are strongly flexed at the middle
and distal phalangeal joints by the contracture of the long
flexor. When the wrist is passively flexed, so as to shorten the
course of the flexor tendons, the fingers can be straightened
without difficulty. Although the flexor contracture pre-
ponderates, the extensors also present some rigidity. In the
leg the rigidity is more nearly equal in the two sets of
muscles, so as to fix the limb in the position of extension.
This rigidity depends on active muscular contracture. It
lessens much during sleep and when the limb is warm. It
can be overcome, for the time, by gentle prolonged extension,
especially if the muscles are simultaneously rubbed. After
some years tissue-changes take place in the muscles, and they
can no longer be extended. Thus we ought to distinguish
from the late rigidity an ultimate structural contracture,
making in all four varieties — ^initial, early, late, and structural
rigidity. The late rigidity coincides with degeneration in the
pyramidal tracts of the cord. Excess of myotatic irritability
accompanies it, as it does the degeneration of spinal origin, no
doubt for the same reason. The foot-clonus and rectus-clonus
can readily be obtained ; in the arm, a tap on a muscle, its
tendon, or the bone to which it is attached, causes a momen-
tary contraction, and sudden tension may develope a clonus
in the fiexors of the fingers, and sometimes in the flexors of
the elbow, and even in the trapezius.

LEOTUEE V.

SYMPTOMS {Continued) : HEMIPLEGIA {Contimied)—CO^YVLSl01S.

Gentlemen, — ^We considered, in the last lecture, the chief
characters of hemiplegia, and the condition of the muscles
in lasting palsy. Some other points regarding the state of
the limbs remain for consideration, the first being the changes
that may occur in their nutrition.

The nutrition of the muscles may be unchanged, even after
the paralysis has existed for years, or slight general wasting
may set in a few weeks after the onset, sometimes slowly attain-
ing a considerable degree, although never comparable to that
in progressive muscular atrophy. The electric irritability of the
muscles may present no change, or a slight increase in irrita-
bility may occur at the end of one or two weeks, and continue
for a few months, to give place to a slight and permanent dimi-
nution. The change is the same to both forms of electricity,
faradaism and voltaism, and is the same in the nerve-trunks
as in the muscles. It occurs chiefly when there is the change
in nutrition just described, and each is probably the conse-
quence of the irritative character of both the cerebral lesion
and the resulting secondary degeneration of the pyramidal
tracts in the cord. Although this degeneration never invades
the motor nerve-cells as a destructive change, it seems to
influence, in slight degree, their nutrition, and therefore
that of the motor nerve-fibres and muscles.

HEMIPLEGIA. Oi

Vaso-motor and trophic changes may be absent or very
marked. They appear to depend in part, like the changes in
muscular nutrition, on the irritative character of the cerebral
lesion ; but there are centres in the cortex that influence the
vaso-motor state of the limbs, and disease of these centres, or
of the downward path from them, the precise position and
course of which are still imdetermined, may be the cause of
considerable disturbance of this character. During the early
weeks there is often increased warmth of the paralysed limbs,
amounting to from half a degree to a degree and a half /^
Fahrenheit, at first uniform, afterwards intermitting. With
this there may be increased redness and lividity, sometimes
with marked oedema, especially if the kidneys are also
diseased. Often there is a tendency to graver trophic
changes : blisters readily form, filled with dark serum ; the
skin sloughs from slight pressure in those parts on which
pressure chiefiy acts in the recumbent posture — ^the gluteal
region, over the trochanter and malleolus. Earely there is
inflammation of joints.

When recovery occurs, power returns in the proximal
parts of the limbs sooner than in the distal parts, and in the
leg before the arm. Indeed, as already stated, some recovery
in the leg is invariable. There is, moreover, more use of the
leg in association with the other, than in its separate move-
ments. The flexion of the foot is that which remains longest
defective, and hence the patient cannot get the toes ofi the
ground in bringing the foot forward in the act of walking,
and swings the leg round. In the arm, the shoulder
recovers before the elbow, and the elbow before the hand.
The extensors remain weak longer than the flexors, and the
supinators longer than the pronators. In rare cases the hand-
movements return first ; and it is singular that these cases
sometimes also present another exceptional feature — the arm
improves faster than the leg. No doubt this peculiarity
depends on a special position of the lesion.

The distribution of the palsy in cases of hemiplegia
depends on the position and extent of the lesion, and certain

forms need special notice. I have already mentioned the
escape of the tongue ou the affected side, when the lesion is
in the medulla, and of the face when it ia in the lower half of
the pons ; that is to say, when the lesion occurs before the
cerebral path from the hypoglossal and facial nudeus has
crossed the middle line, and has become associated with the
path to the limbs. But the eranial iieiren, from the third to
the hypoglossal, in passing from their nuclei to the surface,
may be damaged by disease that damages also the motor
tract. This paralyses the nerve on the same side as the
lesion, but the limbs on the side opposite to the lesion, thus
causing what has been badly termed "alternate hemiplegia."
Certain nerves are more frequently paralysed in this way
than others : the most frequent are the facial, sixth, and third
nerves; less frequently the hypoglossal, auditory, and fifth.
The facial and sixth are sometimes affected together on the
side opposit* to the limbs. The paralysis of the face resem-
bles that due to other diseases of its nerve ; all parts of the
face are paralysed, and there is loss of faradaic and preserv-
ation of voltaic irritabihty. When the lesion is in the cms,
the face is affected on the same side as the limbs, but the third
nerve on the opposite side — on the same side as the lesion.
Do not imagine that this crossed palsy of hmbs and cranial
nerves is invariable when hemiplegia results from disease in
these regions. The lesion may be so placed, or so small, that
the nerves escape. Thus the association of palsy of cranial
nerves on one side, with that of the limbs on the other, gives
us one class of varieties of hemiplegia.

Another class depends on the incomplete extent of the
palsy, the seat of the disease being in the cerebral hemisphere,
where the constituent elements of the motor tract have so far
diverged that its damage may easily be partial. We have
already seen that this must be rare in lesions of the internal
capsule, on account of the proximity of the several paths, and
that it may more readily occur in the white substance, and
moat readily in or beneath the convolutions. The paralysis
may involve only the face, or the arm, or the leg : or it may
involve the fooe and tongue ; face, tongue, and arm ; or face

^

HEMIPLEGIA. 59

and arm. The distribution depends on the relative position
of the centres and paths. Thus the tongue and arm are
never afEected by a single lesion without the face, because
the face-centre and path intervene between the two others.
Similarly, the face and leg are never affected without the
arm, because the centre and path for the arm intervene
between the others. This partial hemiplegia is sometimes
called " monoplegia," distinguished, according to its seat, as
lingual, facial, brachial, or crural, while combinations receive
compound names, as brachio-facial monoplegia. It may
seem to you rather anomalous to call the latter a mono-
plegia, but the whole nomenclature is inconsistent. Strictly,
" monoplegia " should designate double hemiplegia ; but we
call this " diplegia." Thus two " half-palsies " make, not
a " one-palsy," but a " two-palsy," and a " one-palsy " is
less than a " half -palsy."

In these cases of partial hemiplegia, the paralysis never
remains absolute, and usually is not absolute, even at first.
The state of the limb resembles that of a hemiplegia that is
recovering. The coarse movements in the upper part of the
limb are preserved, while the movements of the extremity are
impaired or lost.

The affection of sensation that often accompanies hemi-
plegia I shall describe presently. Before leaving the subject
of motor palsy one curious class of symptoms must be
mentioned. These are the disorders of movement that
sometimes come on some months after the onset. The
rigidity of which I have already spoken is fixed, varying but
little during the waking hours. But the muscular contrac-
tions we are now considering are versatile and changing.
They also vary much in different cases. Sometimes there is
tremor ; fine, quick, rhythmical contractions of the muscles.
Rarely there are slow and rhythmical movements, wider in
range, and chiefiy met with in the hands or fingers. Most
common of all are irregular muscular contractions, irregular
both in time and in degree, rarely quick, far more often slow.
The quick movements somewhat resemble those of chorea, and
hence the term, " post-hemiplegic chorea," has been applied

to the whole olaAs of moA-emeuts — unwisely, because they have
uotliiiig; fo do with chorea, and, moreover, resemble chorea
only iu rare cases. Generally, the movements are far slower
than are seen in true chorea. If not constant, they are readily
evoked by an attempt at voluntary movement, or even by
attention, and by these they are always increased. Inco-
ordination of movement results, peculiar in character — slow,
irregnJir, spreading; movements of the fingers, that have been
compared, not inaptly, to the movements of the arms of a
cuttlefish. " Mobile spasm," it may be convenient!}- termed.
With this there is often some more constant and unchanging
spasm, especially in the flexors of the wrist. The arm is
always involved in greater degree than the leg. In the latter
the effect of the spasm is chiefly to cause inversion of the foot
and over-extension of the great toe ; spontaneous movements
are rare. The ami is usually adducted at the shoulder- joint ;
the elbow is sometimes flexed, sometimes strongly extended.
Often the arm, straightened out, is carried behind the body.
The wrist is frequently flexed; the flngers are usually flexed
at the raetacarpo-phalangeal Joints, extended, and even over-
extended at the others, the spasm preponderating in the inter-
osseal muscles. There may be a subluxation of the extended
finger-jointa, the heads of the phalanges projecting on the
palmar aspect. Thus there is a remarkable contrast between
this spasm and ordinary late ligidity. In the latter the spasm
chiefly affects the long flexors of the fingei-s ; the digits are
bent at all joints, a form of flexion that is employed in coai-se
movements of the limb. In the mobile spasm there is the
" interosseal flexion " just described, the flexion that is em-
ployed in many delicate operations, such as the act of writing.
The continuous action of the muscles often leads to their
overgrowth, and the limb may be actually larger in circum-
ference than that of the opposite side, when it is less in length.
This condition sometimes developes without preceding hemi-
plegia ; and to such a case, in which there was no fixed spasm,
hut only the slowly-changing irregular movements, Hammond
(of New York) gave the name of "athetosis" (= without fixed
position). In the vast majority of cases the condition is n

HEMIPLEGIA — CONVULSION. 61

sequel to hemiplegia. It sometimes comes on after hemiplegia
in adult Hfe, but is far more frequent after hemiplegia in
infancy and childhood, to which it is, indeed, the common
sequel. In adults it has been observed chiefly in cases in
which the lesion was in or near the optic thalamus. Why,
we cannot yet say. In children it does not seem to be
related to any special seat ; it follows disease anywhere in the
motor regions of the hemisphere. The lesion causing the
initial hemiplegia is, however, almost invariably softening,
and not haemorrhage. An analysis of adult cases shows this
clearly ; and in children any other acute lesion than softening
is very rare. These considerations suggest that one element
in its causation may be the partial recovery of nerve-cells that
are damaged, but not destroyed — which recover, but with
disordered functions, — and the greater power of recovery and
greater capacity for derangement during the period of deve-
lopment may be the cause of the special frequency of this
condition after hemiplegia in early Hfe.

From motor palsy, the spasm last considered naturally
leads us to that paroxysmal over-action which causes con-
vulsion. Convulsions are frequent and important symptoms
of cerebral disease. They occur under two conditions, appa-
rently as the result of two different mechanisms. First, they
occur when there is active irritation of the brain-tissue, such
as is produced by inflammation of the brain or membranes,
a growing tumour, or a sudden lesion. Secondly, they occur
in what are termed " stationary lesions," in which the stage
of activity is over, and such structural recovery as may be
possible is taking place, or has taken place. In this case
they are, apparently, due to the imperfect recovery of
damaged nerve-cells, which regain the power of evolving
nerve-force, but not the higher power of regulating its
discharge. By each mechanism, convulsions are produced
most readily when the disease is in the cortex. Stationary
lesions scarcely ever cause convulsions unless they are situated
in or near the motor cortex. Active irritation is most eif ective

when in the same region, but it may eauBe oonvulflions whateTer
be its seat. They are also produced by general increase of intra-
cranial pressure, and by diffuse processes, such as meningitis.
The diagnostic significance of convulsions depends on their
character. They may be general or they may be partial,
either in extent or in commencement. General convulsions
constitute a " diffuse " symptom. They are often due to a
diffuse and widespread morbid process, inflammatory or
degenerative disease away from the motor centres, or to
general increase of intracranial preasm«. Convulsions that
are limited in extent or commencement constitute a focal
spnptom, and indicate disease in or near the motor region,
especially the motor region of the cortex. In general con-
vulsions the I0B8 of consciousness is sudden and immediate;
there is usually no aura. In partial convulsions, consciousness
is lost late, and the patient is usually aware of the local
onset. This local onset is due to the fact that the discharge
begins in the centre irritated — for the face, arm, or leg. If
very slight, it may not spread beyond the one centre in which
it began, the convulsion being confined to the corresponding
part. If more severe, it spreads to all the centres of that
hemisphere, aud the convulsion affects the whole of one side
of the body. If still more severe, the discharge spreads to
the other hemisphere, and the limbs of the other side are also
involved, usually after the first side, sometimes, in the most
severe fits, simultaneously. Consciousness is usually retained
throughout when the convulsion is confined to one limb ;
sometimes when it involves the whole of one side; scarcely
ever when both sides are involved. Different discharges vary
in intensity, and the patient often has slight attacks that are
local, and more severe attacks that begin locally and become
general. The attack usually commences by clonic spasm,
which often becomes tonic if the convulsion becomes severe.
The spasm almost always begins in the extremity of the Kmb.
But it is common for a sensory "aura" in the part to
precede the spasm : the sensation may pass up the limb first
affected, along the side of the trunk, and down the second hmb
affected, and only then may spasm be added. It is as if the

CONVULSION. 63

discharge commenced in the sensory cells of the cortex, passed
like a ripple through these sensory centres, and only when it
reached their limit was deflected to the motor cells. In the
very slightest attacks the sensory aura may be accompanied, not
by spasm, but by the opposite condition — sudden powerless-
ness of the limb. The influence of the sensory discharge on
the motor cells may thus be to inhibit them, if it is of very
slight degree — another instance of the relation of inhibition
and discharge mentioned on p. 47. Special sense aurse are very
rare in organic disease ; when they occur they indicate that the
disease is in or near the part of the cortex that subserves the
corresponding functions. Thus, I have met with a case in which
a flash of light was the aura of fits due to a timiour of the
occipital lobe ; and another, of a timiour beneath the temporo-
sphenoidal cortex, in which the soimd of bells was the aura.

A convulsion leaves behind it a transient weakness in the
part convulsed, probably due to exhaustion when the spasm is
severe, or to motor inhibition when the spasm is slight or the
discharge is limited to the sensory cells, sometimes perhaps
to both mechanisms. The weakness after a unilateral fit
may resemble slight hemiplegia, and, if the convulsions
recur at short intervals, the residual palsy accumulates until
it may amount to absolute powerlessness of the side, with
increased knee-jerk and foot-clonus. It gradually passes
away after the convulsions are over.

The characteristic, then, of the convulsions of organic brain-
disease is their local commencement. Whether the fit remains
limited to the part in which it commences, or spreads to other
parts, even the whole body, is a question of degree. Moreover,
a local aura, without convulsion, has the same significance as
local spasm. It indicates that the discharge commences at one
part of the brain, that there is at that part a morbid state, and
it is thus a focal symptom. Convulsions that are general from
the first are often due to, and symptoms of, organic brain-
disease ; but they derive their significance from associated
symptoms, and not from their character. Without such
symptoms they suggest idiopathic epilepsy, not the organic
brain-disease that local commencement suggests. I say

64

mggests, Tjeoanse there is sometimes a local commencement in
idiopathic epilepsy. This is, however, rare, and you ■would
not think of idiopathic epilepsy in such a case unless you had
ascertained that other symptoms of organic brain-disease
were absent, and you could not feel confident, unless the con-
vulsions had existed alone for a considerable time, or there
was a strong family tendency to the idiopathic disease.

The first oonvulsions from organic disease are sometimes
excited by a cause outside the central nervous system, a cause
that may seem to be adequate to account for them. This is
a very important point. Remember that the apparent cause
of a fit is scarcely ever more than its excitant — an excitant
that is effective only because there is a predisposition ; and the
predisposition ha the important matter to be sought out and
to be treated. The spark would be harmless unless it fell
on gunpowder. The predisposition may be sometimes an
inherited tendency of the nervous system, or it may be an
acquired state of morbid irritability, such as forms part of
the constitutional disease we call "rickets," or it may be
a brain disease that has not reached such a degree as to
cause pronounced symptoms. For instance, a child was
brought in here who had swallowed a slate pencil, and then
had an attack of general convulsions. For this the slate pencil
seemed an adequate cause. It was passed by the bowel, and
the child seemed well. But six weeks afterwards she was dead,
and the cause of death was a large infiltrating glioma of the
pons, which must have existed at the time of the convulsion,
and no doubt gave rise to the predisposition. As in this
ease, the convulsion so esoited is usually general. But only
a few weeks ago, you may remember, we had a man in Ward
rV., whose history showed that a convulsion beginning locally
may be excited by a local cause, even though it ultimately
depends on organic brain-disease. The man, when apparently
well, struck his left arm against an iron hook, and a few
hoiurs afterwards had a fit which began in this arm, and
was heralded by a pain at the part struck. He afterwards
bad other similar fits. It seemed like a ease of what is
termed "reflex epilepsy" — a disease, by the way, muoh

CONVULSION. 65

more raxe than you may imagine from books. But one day
lie had a fit which began in the foot, and not in the arm.
Then he developed headache, double optic neuritis, and
hemiplegia ; and when he came in here, he presented the
characteristic symptoms of a tumour in the upper part of
the ascending frontal convolution. The blow on the arm
had determined the time and place of an explosion, of which
the real cause was the organic brain-disease. Such a case is
the converse of the arrest of a fit, beginning locally, by a
ligature roimd the limb, when the fit is due to organic
brain-disease, and the ligature can only stop the fit by acting
on the centre in the brain.

Remember, then, that convulsions should not be lightly'
dismissed from consideration because the fit succeeded an
exciting cause.

Sufferers from organic brain-disease who are of the age
and sex in which the predisposition to hysteria exists, may
suffer from attacks of hysteroid convulsion. It is not
surprising that so potent a disturbing influence should evoke
into activity a tendency from which few women are altogether
free. But the fact is of extreme diagnostic importance,
because, when one of a set of symptoms is unmistakable in
character, it is natural to take it as an index to the series.
You should never do so, gentlemen, imtil you have satisfied
yourselves that no symptom is certainly of a different nature.
I insisted on this in speaking of the diagnosis of diseases of
the spinal cord, and it is equally true of those of the brain.
Both acute and chronic disease may lead to the strange dis-
turbance of function to which we give the name hysteria, and
which we might just as well call, as did our forefathers,
"fits of the mother." I have seen it, for instance,
many times in cases of cerebral tumour, many times in
tubercular meningitis, and once at the onset of an attack of
embolic hemiplegia. It is a very frequent consequence of
the defective development of the brain that results from
infantile lesions. Some of you may remember a curious girl
who attended here for a long time, whose powerless and

68 LECTURE V.

withered arm was the rehc of a severe infantile hemiplegia.
She Buffered from unilateral epileptiform eonvulaions, and
also from pure hysteroid fits of intense severity, as well as
from laryngeal spasm, phantom tumour, and various other
eymptoms of the same class.

P

Tonio spasm, in the form of mnsoular rigidity, occurs as a
ekronio symptom chiefly after hemiplegia, and as an acute
and subacute symptom in irritating lesions, especially in
inflammation of brain and membranes, either primary, or
secondary to necrotic softening. It is almost always one-
sided. Severe tetauiform spasm is rare. It is generally
paroxysmal, and has been met with chiefly in disease of the
cerebellum, hut only in cases of tumom-, and it is probably
due, not to the damage to the cerebellum, but to the pressure
of the tumour on the pons. Similar spasm may be caused
by tumours of the pons. Forced movements, as a tendency
to rotation, are extremely rare. They resemble those pro-
duced in animals by inj'iuy to the semicircular canals or
cerebellum, and have been observed chiefly when disease
involved the middle cerebellar peduncle. Of their precise
meohanism we are still ignorant. Pine tremor is rare
except after hemiplegia, but sometimes attends muscular
weakness in chronic disease. It is without speeial sig-
nificance. Inco- ordination of movement is also rare except
after hemiplegia. Insular sclerosis of the brain and cord is
attended by jerky inco- ordination, sometimes wild in its
irregularity and in the extent of its range. It is important
to know that a precisely similar form of inco-ordination is
sometimes met with in cerebral tumour. I have seen it in
oases of tubercle of the pons Varolii and cms cerebri, when
the tumour has compressed the motor tract. There is usually
hemiplegic weakness ; and the movements of the leg, as well
as those of the arm, may be irregiilar. Charcot beUeves that
the mechanism of this inco-ordination in disseminated sclerosis
is an imequal morbid resistance in the nerve-fibres passing
through a sclerosed area, and a similar effect may, conceiv-
ably, residt from compression by a tumour.

LECTUEE VI.

SYMPTOMS (Continued) : DISTURBANCE OF SENSATION-
AFFECTIONS OF SIGHT.

GrENTLEMEN, — ^From the motor symptoms that occupied
our attention in the last two lectures, we pass to the corre-
sponding disturbances of sensation. The best instrument
for testing sensibility is a simple one, a quill pen — the feather
for touch, and the point for pain. We will consider first the
loss of sensation that is analogous to the motor palsy, and
often attends it. Hemiplegia may exist without any sensory
loss, or with every degree of this loss. Complete hemianses-
thesia may exist alone, or may be combined with every
degree of motor palsy. It is rare, however, for the two to
exist in high degree : usually a considerable degree of one
is combined with a slight degree of the other. I am speak-
ing now and always of organic disease, and have nothing to
do, beyond a passing reference, with the mysterious hemi-
ansBsthesia that occurs in some cases of hysteria.

The one-sided loss of sensibility may involve all forms of
sensibility — of touch, pain, temperature — or may involve one
more than the others. In its complete form it extends up
to the middle line, the absolute loss, however, usually stopping
short of the middle line by a centimetre or so. It involves the
mucous membranes as well as the skin. It always depends
on interference with the sensory path, the course of which I

F 2

described to you (p. 15) ; "but if the lesion is in the pons, the
parts supplied by the fifth nerve escape. The most frequent
seat of disease causing hemianEssthesia is the posterior part
of the internal capsule, between the posterior extremities of
the optic thalamus and lenticular nucleus. Disease here, you
■will remember, may involve the special senses on the same side
as common aensibility, the affection of sight being, however,
hemiopia, due to arrested conduction from the haK of each
retina. Although the destination of the sensory path seems
to be the cortex under the parietal bone, hemiautesthesia only
results from cortical disease when this is very extensive, and
then (as the case related on p. 16 shows) the special senses
may be involved, and instead of hemiopia we may have loss of
sight in the eye on the anesthetic side, and perhaps hemiopia
also in the eye of the same side, if the disease involves the
occipital as well as the parietal lohe (see p. 23, note).

The slighter forms of defect may be characterized, not
by any absolute loss, but by slight qualitative change. A
patient, for instance, often avers that there is a difference
throughout one side, that a touch or a prick does not feel
the same as on the other side, although there is no place
at which the slightest touch is unfelt.

P

The second form of loss of sensation often accompanies
hemiplegia. The loss exists chiefly or only in the hmbs, and
is greatest in, often confined to, the extremities. Tactile
sensibdity is lost in greater degree than sensibility to pain,
and there is often an inability to recognize the position of the
hand or foot, even when the skin is perfectly sensitive. Thus,
the patient's eyes being closed, the hand and fingers are
moved about, and finally held in some posture which the
patient is asked to describe, or to imitate with the other hand.
If there is no tactile loss, the fingers should be firmly grasped
so that the direction of pre^ure may not inform the patient
of the posture. This should be repeated several times,
since too much weight must not be laid upon a single
error, especially if the patient is unintelligent. It is
remarkable that iu some cases in which the patient oan

LOSS OF SENSATION. 69

feel the slightest touch on the hand he has not the least
idea of the posture in which it has been placed. This loss
occurs in disease of the motor cortex. It depends, accord-
ing to Munk, on the loss of the structures that subserve
conceptions of movement. We cannot yet say, however, that
it does not result from disease elsewhere. Indeed, some of
you may remember a case of hemiplegia that was in the
hospital a few months ago, in which this loss was as distinct
as it can ever be in an unintelligent patient, and the cortex was
intact, the lesion being confined to the internal capsule and
corpus striatum. Hence the diagnostic value of the symptom
as evidence of cortical disease is probably not great.

It is a curious fact that lesions of the brain occurring in
infancy or early childhood seem never to cause permanent
loss of sensibility, although they must sometimes involve
the sensory path or centres. This fact shows that, in the
growing brain, compensation by other parts, perhaps by
the other hemisphere, is possible in regard to this function
in very complete degree.

The hemiansesthesia that occurs in hysteria may be mis-
understood and ascribed to organic disease, but careful
attention to the other symptoms in the case will generally
prevent error. Remember that in hysteria one-sided loss of
sensibility, although usually complete, is not always so ; the
special senses, and even the head, may escape. If it is com-
bined with motor palsy, the loss of feeling may be much
greater in the weakened limbs than elsewhere. The risk of
error is greater in such cases than it is when the hemianses-
thesia is complete and the special senses are affected — ^vision
as "crossed amblyopia." Perfect as is the correspondence of
this sensory loss to that which may result from organic
disease of the cortex, the slight risk of erorr that there is
may be avoided if you remember that the symptom can be
produced by organic disease only when this is very extensive
— so extensive that its nature could not admit of question. If
you doubt whether there is organic disease, you may feel sure
that there is not. In the only situation in which a small lesion

70 LECTURE VI.

ean cause hemiansesthesia with affection of the special senses
(the posterior part of the interna! capsule), the affection of
sight ia always hemiopia.

Perhaps the greatest risk of ascribing hysterical loss of
sensation to an organic cause is in the cases of infantile lesion
of the brain that I hare just mentioned. I told you, in the
last lecture, how .prone the female subjects of such disease are
to develope hysteria. If you are not aware that such lesions
do not permanently impair sensibility, you may easily ascribe
hysterical bemianEssthesia in such a case to the organic disease.
It is one of the most subtle of the many traps that hysteria
delights to set for the unwary diagnostician. I ha*l myself
to pay for my experience. Some years ago a girl came to
me with infantile hemiplegia of the ordinary type, with
shortened limbs, and mobile spasm in the arm. She com-
plained of no symptoms suggestiTe of hysteria. On testing
sensibility I found that the whole of the paralysed side was
anfBsthetic ; the special senses were blunted on that side,
vision was much impaired, and colour-vision was lost. Here,
I thought, are two most interesting things : first, thei-e is a
lasting loss of sensibility from a lesion of the brain in
infancy ; and secondly, there is crossed amblyopia from
organic disease. I made most careful notes, and told her
to come again in a week. She did so ; and on the paralysed
side sensation was now perfect, and aU the loss of feeling
had gone over to the other side! Only a few months ago, in
one of the medical papers, I saw an account of a similar case,
which was published as hemiansesthesia of organic origin.

SjinptomB due to irritation of the sensory tract or centres
are not uncommon i;i central disease. Tinghug, formication,
and the varied sensations called "numbness " ai-e frequently
associated with hemiplegia, as prodromata and as accompani-
ments. They are common both with and without actual loss of
feeling. When the lesion occupies the motor centres or path,
these sensations, like the aniesthesia in the same cases, occupy
chiefly the extremities. Such sensations, extending over the
whole of one side, up to the middle line, attend disease
in or near the sensory path, and may herald or accompany

^

SENSORY SYMPTOMS. 71

hemiansBsthesia. The ansesthesia may be transient, and the
sensations persistent, no doubt because the lesion is so placed
near the sensory path or centres as to irritate but not to inter-
rupt them. In the same class of cases there may be persistent
pain in the limbs, usually dull and wearying. The patient
whose fields of vision are represented in Fig. 8 suffered severe
pains of this character for many years, the result of a lesion
which caused transient hemiplegia and persistent hemiopia.

Paroxysmal sensations of tingling, " pins and needles," or
pain, may result from such discharges as, in motor structures,
cause convulsions, and the sensory discharge often accompanies
the motor. I spoke of these sensations in the last lecture.
It is also very important for you to know and remember that
such one-sided sensations of tingling, etc., may occur as part
of the strange phenomena of migraine. They are then more
deliberate than those that herald a convulsive attack or
constitute a minor seizure, lasting for half an hour or an
hour. When on the right side, aphasia often attends them.
Followed, as they are, by violent headache, they may cause
much alarm, not only to the patient, but also to his medical
adviser, if the latter is imaware of the occurrence of such
sensory disturbance in this association. If the patient has
not had such an attack before, he is certain to have suffered
from paroxysmal headache, and probably froin slighter sensory
symptoms, especially in vision; from these you may feel
sure of the nature of the attack.

We pass from the disturbance of common and tactile
sensibiHty to the symptoms that depend upon disturbance of
the nerves of special sense. These are cranial nerves, and
it will be most convenient to go through the cranial nerves
seriatim, considering the symptoms within the range of their
functions in the anatomical order, which is nearly the order
we adopted in the description of the anatomical relations of
the nerves. Those relations you must bear in mind, if you
would imderstand the important symptoms that are produced
by disease of the nerves, or of the central tracts that continue
their path to the cortex.

"We commence, then, wifli the nerve of smell. Remember
that the olfactory nerve subserves not only the sensations that
we recognize as odoura, but also those that are termed flavours.
We oall the sensation an odour when its cause reaches the
oliaotoiy membrane by the anterior nares, a flavom- when ita
oause enters the nose by the posterior nares. In the latter
ease the sensation is combined with a true gustatory sensation
(of sour, sweet, bitter, etc.) from the tongue and fauces, and
the two are so blended that we seem to taste flavours when
we really only smell them. Hence those who have lost smell
always say that they have also lost taste, although you will
find, on trial, that the true gustatory sensations are unim-
paired. In examining the sense of smell you must employ
only odorous substances that are not pungent; i.e., do not
iiTJtate the fifth ner\'e, or the patient may perceive that which
he cannot smell, and the result is eonfusing. Loss of smell
is an infrequent symptom of brain disease. Its most common
cause is disease of the olfactory mncoua membrane, polypus,
chronic catarrh, and the lite, the absence of which must always
be ascertained before the symptom is allowed significance.
Mechanical injury, by damaging the delicate filaments that
come from the olfactozy bulb, is another occasional cause.
Diseases of the anterior fossa of the skull, tumour, aneurism,
meningitis, sometimes cause it, aud it may result from the
pressure on the bulbs in extreme internal hydrocephalus.
Prom central disease it is very rare, except in association
with complete hemianiesthesia ; it is then on the side opposite
to the lesion. It probably may be produced also by disease
in the temporo-sphenoidal lobe, near the iimer part of the
fissure of Sylvius, and will be then on the same side as the
lesion. If occurs occasionally in degenerative diseases, as
general paralysis of the insane, perhaps in consequence of
an atrophy of the ner\-e analogous to that of the optic nerve.
Subjective sensations of smell are almost confined to func-
tional diseases (as the aura of epilepsy, etc.), but have been
noted from tumour of the temporo-sphenoidal lobe.

OPTIC NERVE. 73

Disturbed function of the optic nerve is a very common
symptom of brain disease. In acute lesions it is generally
due directly to the cerebral lesion ; in chronic disease it is
often the result of optic neuritis, and is thus a secondary
effect of the brain-mischief, of significance chiefly as to the
nature of the disease. In almost all cases, however, an
ophthalmoscopic examination is necessary to ascertain whether
the affection of sight is of intra-ocular origin, before its sig-
nificance can be determined. There is only one form of
impairment that can be referred with certainty to central
disease, and that is hemiopia. Even in acute lesions of the
brain, which do not, as a rule, entail optic neuritis, coincident
retinal changes, such as albuminuric retinitis, haemorrhage,
and embolism, sometimes cause impairment of vision, the
origin of which can also only be ascertained by the ophthal-
moscope. If optic neuritis is foimd, we are not justified in
immediately ascribing the impairment of sight to its effect.
If the visible neuritis is slight in degree it will not accoimt
for affection of sight. The latter may be due either to a
more considerable retro-ocxilar inflammation of the nerve, or
to the central disease, and between the two we can only
decide by the symptoms.

I have already mentioned the chief points in the anatomical
relations of the optic nerves that determine the form of loss of
sight from disease in the several parts of the visual path.
Loss of sight of one eye means an affection of its nerve be-
tween the eye and the chiasma, i.e., in the orbit, at the optic
foramen, or within the skull. Temporal hemiopia — ^loss of the
outer half of each field of vision — ^means damage to the middle
of the optic chiasma, affecting the fibres that cross from the
nasal half of each retina, and leaving imaffected those at the
sides of the chiasma that do not cross. Its most common
cause is a txmiour, distension of the third ventricle, and in-
fiammation. Affection of only the non-decussating fibres,
by damage to each side of the chiasma, causes nasal hemiopia,
but is extremely rare. Disease anywhere in the optic path,
from the chiasma to the occipital cortex, causes hemiopia, which
may be complete or incomplete, but is always symmetrical,

p

74 I.ECTTTKK VI.

although not always mimitely symmetrical. When incom-
plete, a part only of each half-field is hlind. Amhlyopia of
one eye, with eonsiderahle peripheral restriction of the field
of vision, occurs from extensive disease of the cortex of the
opposite hemisphere, and perhaps from a small lesion in
the angular gyms. As I have told you {p. 24), there is
usually loss of colour-vision, and there is also aUghter
reatriction of the fields (white and colour) in the eye on
the same side as the disease. When caused hy acute non-
progressive lesions, this loss usually boou lessens, perhaps by
compensatory action of the centre iu the other hemisphere, or
of the undamaged part of the affected centre. Thus, affection
of sight of one eye may he due to disease at either extremity
of the visual arrangement — the optic nerve, or the highest
cortical centre. The two are distinguished hy the following
indications: (1) the reaction of the pupil is lessened in disease
of the nerve, and not in disease of the hemisphere ; (2) the
other eye suffers in a similar hut slighter way in cortical
disease ; and (3) the associations of the two are wholly differ-
ent, cortical disease being accompanied hy hemiauEesthesia and
no aiEeetion of the cranial nerves ; whereas, in disease of the
optic nerve, hemiantesthesia ia always absent, and the motor
nerves to the eyeball are very often involved. Remember,
however, that for one case of crossed amhlyopia and hemi-
auEesthesia from organic disease, you will see many that are of
functional origin, and the evidence of an organic lesion mtist
he very clear before you can ascribe the symptom to this
cause.

A simple peripheral restriotion of the field of vision occurs
also in optio nerve atrophy, both in simple atrophy and
in that which follows neuritis. In the latter the fields
are often irregular; sometimes there are islets of loss
(" scotomata," as they are termed) within the field, and such
islets may vary for different colours. A central defect ia a
consequence of damage to the fibres in the axis of the nerve.
It is common in tohacco-amhlyopia, but is scarcely ever met
with in brain disease.

In searching for these defects of sight you should first aacer-

AFFECTIONS OF SIGHT. 75

tain whether there is any considerable error in the refraction
of the eye. A slight amblyopia, which you might otherwise
ascribe to an affection of the optic nerve, may be due to this
cause. It is beyond my present task to describe the methods
by which the examination may be made with precision, but for
the purpose in view a rough estimate may be formed in the
course of the ophthalmoscopic examination. When you throw
the light into the eye, as for the indirect examination, if you
can see the retinal vessels distinctly, the refraction is abnormal :
move your head to one side, and the vessels, thus seen, appear
to move : if this movement is in the same direction as your
head, the eye is hypermetropic ; if in the opposite direction, the
eye is myopic. Tou may further ascertain the degree of each
defect in the direct ophthalmoscopic examination, by observing
the strength of concave glass necessary for clear vision of the
fundus if the eye is myopic, and the greatest strength of
convex glass that does not blur the image if the eye is
hypermetropic. Of course if your own eye is of abnormal
refraction you must allow for this. In the further examina-
tion of vision each eye must be separately tested. Acuity
of vision is ascertained by test-types, numbered according to
the distance in feet (or metres in the case of Snellen's test-
types) at which the type should be distinct. The result is
expressed in the form of a fj'action, of which the denomi-
nator is the number of the test-type, and the numerator the
farthest distance at which the type is read by the patient.
Thus, ^ means that the type which should be read at a distance
of six feet can only be read at one foot. Colour- vision is
examined by the method of comparison (with wools, etc.), for
an account of which I must refer you to books on ophthal-
mology. It may also be tested by asking the patient to name
colours — a method chiefly valuable when you wish to compare
the colour- vision of one eye with that of the other. By the
method of comparison you escape the errors arising from the
oommon inability to name colours with precision, and from
the uncertainty of the natural appreciation of colours, and
of the sense attached by the patient to the names he gives.
This element, which we may term the personal colour-equa-

tion, does not come in when we merely compare the sense-
impreasions of one eye with those of the other, and we may
therefore, in this oase, ask the patient to name the colours,
and often learn much regarding his perception of colour that
can he ascertained in no other way.

The examination of the fields of vision ia of especial import-
ance in the diagnosis of hrain disease. For an exact examina-
tion it is necessary to use a " perimeter, ' ' an instrument in which
an arm, in the form of a quadrant of a circle (graduated in
degrees), rotates on one extremity, and thus may he made to
occupy successively the various radial arcs of an imaginary
hemisphere, of which its pivot is the centre. The patient's eye
heing opposite and looking at the pivot (his other eye heing
closed), a small white or coloured ohjeet is moved along the
oiTU in each radial position, and the point at which the ohjeet

P

HoiiMAL Fields.

at the tisiog point ; the email circle indicates ttie blind spot
(optic nerve entrauce) ; R, right ; L, left ; T, tempoml dv outer side ;
N, naaal oriunetside. The radii and concentric circles are each 30° apart,
ceases to he seen is the limit of the field in that direction. The
results are marked on a chart, which consists of radial lines
(corresponding to the positions of the arm) and concentric
circles (corresponding to the divisions on the arm). A Hne
joining the points in each radial line, at which the object
ceases to be seen, indicates the peripheral limit of the field of
vision. This, as already stated (see p, 20), is not a circle,
heing less extensive inwards than outwards, and above than
below, on account of the projecting nose and eyebrow, and
the influence of these on the fmictions of the corresponding
parts of the retina. In Fig. 18, which represents an average

AFFECTIONS OF SIGHT. 77

normal field, the circles and radii are not represented
beyond the limits of the field. These circles and radii may
be as numerous as you like ; in the figure only those at 30°
distance apart are represented. The size of the object may
be a centimetre or half a centimetre square. To ascertain the
colour-fields, a coloured object must be used, and the points
noted at which the patient ceases to see the colour, not the
object. The latter can still be seen outside the region in which
the colour is recognizable, the fields for colour being smaller
than that for white, and their order, beginning with the
smallest, is violet, green, red, yellow, and blue. An examina-
tion with the perimeter requires time, and need only be
employed when you have reason to suspect that there is a
limitation of the field. You may ascertain whether there
is any considerable defect by a much rougher method of
examination. Let the patient stand opposite to you, and
about two feet away. Make him place his hand over the eye
you do not wish to examine, and keep the other fixed on your
eye that is opposite his, your other eye being closed. Next
place your hand, midway between yourself and him, in
various places towards the limit of your own field of vision,
and ask him if he sees it; move your fingers, if you like, and
ask him if he sees them move. Still better, place a small
piece of white paper on the end of a dark-coloured stick (a
penholder answers well), and hold the paper in various
positions all round the outer part of the field, or nearer the
centre if you suspect any central loss of vision, holding it
so that the light falls well upon it, and the surface, not the
edge, is towards the patient. In this method the patient uses
your own eye as a fixing point, and you are able to see at
once if he looks away from the fixing point and at the object,
as he is almost sure to do at first. You check his field of
vision by your own, and do not move the object into positions
in which it is beyond the natural range of sight.* A still
rougher method of ascertaining that there is no symmetrical

* For testing the colour-fields in this manner, Messrs. Pickard & Curry
make small coloured metal discs, that can be fixed on a pen, and carried in an
ophthalmoscope case.

78 LFxrvvRH VI.

hemiopia is the following: — Let the patient stand opposite to
you with hoth eyes open, looking at you. Hold up both
your hands, one on each side, as far apart as you can well see
them. Then put them down, and ask him if you held up
one hand or two. Do not ask him this while the hands are up,
or he is almost sure to look first at one and then at the other,
and say " two " If both hands were seen there is no defect
in the outer half of either field, and therefore no ordmary
hemiopia, since, m this, one outer half must he defective

Eemember that the subjects of hemiopia are not always
conscious of it, espetially when the hue of hhndness does
not go ver\ near the fising point, the loss is often un-
noticed One Tvoman with such hemiopia was indignant at
the suggestion that she had anj defert of sight, declai

The Bhudliig represents the blind part the aval oatlme of each figure
the arerage normal field The asterisk ib the fixing point.

that she " could see her husband coming across the common
before any one else could " In another patient the delect was
not discovered until the nurse noticed that the man never ate
his potatoes at dinner. They were always put on the same
side of his phite, and he never saw them. The same patient
once demonstrated his hemiopia to a gentleman in the street,
who was walking with a lady. In the patient's cfEort to
avoid the lady he walked right on to the gentleman. The
subjects of this defect often hold the head inclined towards
the blind side, ao as to bring objects further into the remain-
ing part of the field, and thus see the relations of objects
better. A hemiopio cabman was thus able to drive his

AFFECTIONS OF SIGHT. 79

haoBom about London quite well But if he wanted a fare
he had to go on a rank, because, if he looked about him, he
was sure to run into something '^

The chief facts regarding the form of hemiopia are five,
and I have already alluded to some of them in speaking of
the indication they aSord of the relation of the optic path.
The firat is that the division ma'v pass through the fixing

point, or may diverge so as to leave it within the region of
vifiion (Fig. 13). Secondly, the line of division is often
slightly irregular : the divergence that leaves the fixing point

Fio. IB. — Partial Right Hemiopia from DiauAsE of the L
Hbmispherb, the Loss being heably Quadrantic. t
coirwpondence of the shape of the blind area in each field.)

in the region of vision may commence just above, and end just
below the fixing point ; or may begin some distance above
and extend below this. Thirdly, the line of division often
inclines to one side or the other, above and below (as in
Figs. 14 and 17), and this inclination may be in opposite

directions above and Iwlow, so aa to give rise to on oblique
heraiopia (Fig. 15). All these variations are probably diie
to individual variations in the decussation of the optic nerves,
and not to the seat of disease. The next fact is that the
hemiopia may be incomplete, only a portion of each half
being lost. It is utnially a segmental defect ; often an irre-
gular quadrant, as is shown in Fig. 16. This partial losa is
due to partial destruction of the visual path or centre, aud
depends on the limited extent of the lesion (seep. ii^). Lastly,
the hemiopia may be accompanied by concentric restriction of
the remaining half-fields, greatest in the eye on the side oppo-
site to the lesion, and sometimes confined to this eye. An
instance is shown in Fig. 17. It is probable that this occurs
only when the disease is in the cerebral hemisphere, and not

F\SF UF TH

ERir

HT Cfkfbbai Hbmi

TIliCTUIV

THE

EEaAiNiNo Half

Left Eye

HAV

IN THE R7RHT

when the tract is di'^eased, and that the restriction is due to
an interference with the iugheist visual centre, or with the
fibres passing to it The restiiction is not alwajs present
even when the disease is m the hemisphere You must
remember, however, that concentnL restriction of the fields
may result from optiL neuntis, and it maj then be even
greater than that which results from the cerebral lesion
The only difference between the characters of the two is that
the restriction from neuntis is more nearly equal m the two
eyes than is that from central disease.

Transient loss of sight occurs in some functional diseases
of the brain, but its paroxysmal character precludes almost

AFFECTIONS OF SIGHT. 81

all danger of mistake. In epilepsy the loss is complete,
but is usually followed instantly by loss of consciousness.
In migraine, hemiopia is common, and total loss is rare, but
the symptom lasts, as a rule, only a quarter or half an hour.
The affection of sight that occurs in hysteria I have already
mentioned; there is usually considerable amblyopia of one eye,
with sHghter amblyopia of the other, and extensive impair-
ment of the other special senses and cutaneous sensibility on
the side of greatest visual loss. The distinction I have just
described to you. In hysteria there may be also complete
loss of sight of one eye, the other being unaffected ; but this
is rare. The perfect action of the pupil sufficiently distin-
guishes it. It is doubtful whether hemiopia is ever of
hysterical origin ; and this is strange, because, in migraine,
hemiopia is common. Apparently the two affections are on
different functional levels, and keep to them. Persistent
hemiopia is almost always due to organic disease, and its
significance is therefore decided. Of a large number of cases
of hemiopia of which I have notes, there is only one which I
think may have been hysterical.

Irritation-symptoms in the function of the optic nerves
are rarely due to organic disease, while they are common in
functional disturbance. Intolerance of light occurs in menin-
gitis, but is rather a cerebral than an ocular s3miptom —
light seems to distress the head rather than the eye. True
photophobia is scarcely known in brain disease, or in diseases
of the optic nerve. Visual discharges, subjective lights or
colours, occur in epilepsy and in migraine ; in the former,
flashes or points of light are common; in the latter, the
zigzag "fortification" appearance is characteristic. Disease
near the visual centre in the cortex may cause subjective
sensations of light, but only as s3miptoms of a discharge
that quickly bursts into a convulsion.

G

LECTURE VII.

SYMPTOMS {Cmttimied) : OCULAR NERVES— FIFTH NERVE-
FACIAL ITERYE.

Qtntlemen, — ^We may conveniently consider together the
symptoms that depend on the three cranial nerves that
supply the eyeball muscles — ^the third, fourth, and sixth-
All supply external muscles ; the third nerve also some
internal muscles. Paralysis of the external muscles is
indicated hy symptoms of five kinds: (1) limitation of
movement; (2) non-correspondence of the direction of the
two eyes, i.e., strabismus ; (3) double vision ; (4) erroneous
projection of the field of vision of the paralysed eye ; (5)
secondary deviation of the unaffected, eye. The defect of
movement is always in the direction of action of the
paralysed muscle, and ia termed the " primary deviation,"
It is most conspicuous when the unaffected eye " fixes " the
object, and the affected eye is prevented seeing it by the
interposition of the hand, or a piece of paper, in such a
manner that the eye can still be observed. The " secondary
deviation" is an excessive movement of the sound eye,
when this is prevented seeing the object at which the affected
eye looks. If then the interposed hand be moved so as to
cover the affected eye, the sound eye, to " fix " the object,
has to move back again, and the degree of backward move-
ment indicates the degree of previous excess, that is, of
secondary deviation. Both primary and secondary deviation

OCULAR NERVES. 83

depend on the circumstance that the muscles of the two
eyes reserve an equal amount of innervation from the
centre. That which suffices to move the sound eye into
a given position is insufficient to move the affected eye
into the corresponding position, and the innervation neces-
sary for this causes an excessive movement of the sound eye.
Thus, the primary deviation being a defect, the secondary
deviation is an excess ; they are in opposite directions, but
both are in the line of action of the affected muscle. In
slight palsy the secondary deviation is often more readily
observed than the primary deviation. The patient habitually
fixes with the imaffected eye, and hence the primary devia-
tion, the paralytic defect of movement, occurs whenever the
eyes are so moved as to bring the affected muscle into action.
The difference in the direction of the two eyes constitutes
strabismus, and from it there results double vision. The
paralytic strabismus may be convergent or divergent, or
there may be a difference in the height of the two eyes,
a,ccording to the muscle affected. The strabismus is dis-
tinguished from that due to muscular spasm by the fact that
the latter is the same in all positions, whereas the former
only occurs in the positions necessitating the action of the
affected muscle ; in spasmodic strabismus no secondary devia-
tion can be obtained. Double vision is conmionly present in
paralysis, at least when this is recent, and absent in the
common spasmodic strabismus. This difference does not
depend on the nature of the two affections, but on their
duration. In chronic deviation of the eyes, from whatever
cause, the patient learns to neglect the image seen with the
affected eye (termed the " false image "), and to attend only
to that seen with the sound eye (" true image "), and may be
quite imaware of a diplopia which is at once conspicuous to
him if a coloured glass is placed before one eye so as to tint
one of the images. It is best to place the coloured glass
before the sound eye. When the images are so near together
that they overlap, the image appears to be blurred rather
than double, but the coloured glass distinguishes the two.
If a coloured glass fails at first to reveal the double image,

G 2

the observer's hand may he placed before first one and then
the other eye, and the object will appear to change its
position as well as its colour with the change in the eye
obscured. Double vision may he "mossed" or "simple."
In crossed diplopia the image in the left eye is seen to the
right of that in the right eye. In simple diplopia (usually
called " homonymous " or " same-named ") the image in the
left eye is seen to the left of the other. When the stra-
bismus is divergent, the diplopia is crossed ; when convergent,
the diplopia is simple. If you will mate a diagram for
yourselves of the eyes in the two positions, and of the rays
of Hght from an object, you will understand this without
difficulty. Should you find it hard to keep in mind the
character of the diplopia in the two cases — and these simple
alternatives often give much trouble to the student —
remember that when the prolonged axes of the eyes would
cross, the double vision is not crossed.

The receut paralytic diplopia exists only in positions of
the eyes needing the contraction of the weak muscle, and
the farther the object is moved in the direction of action
of the muscle, the farther apart are the two images. In
old-standing cases some secondary contracture of the anta-
gonists may give rise to diplopia in other positions, and even
at rest. In many positions of the eyes the two images are
not parallel. This depends on the complex associated action
of the oblique and straight muscles, with which you are
doubtless already familiar. If a paralysed straight muscle,
in a certain position, has a tendency to rotate the globe,
which tendency is normally counteracted by one of the
oblique muscles, the latter,, producing its effect alone, causes
an abnormal rotation of the eye.

The "erroneous projection of the visual field" is not
quite so abstruse a subject as some old associations vrith
the word " projection " may lead you to fear ; and it is a
question of much interest. We judge of the relation of
seen objects to each other by the relative position of their
images on the retina, i.e., by their relative position in the
visual field ; but we judge of their relation to our own \

o our own liadi^

OCULAR NERVES. 85

by the relation to it of the whole visual field. This depends
on the position of the head and of the eyes, and we know this
by the degree of innervation of the muscles that move the
head, and especially of those that move the eyes. We are
only now concerned with the latter. When the innervation
of the ocular muscles is at a minimum, the eyes are in mid-
position, and we know, to use popular language, that an
object at which we are looking is opposite our face ; that is,
that a line from the centre (fixing point) of the field of vision
to the macula lutea would stand at right angles to the plane
of the face. If we turn the eyes to one side, we know
that an object now in the centre of the field is to the
side of the position of the former one ; how far to the
side, we judge by the degree of movement of the eyes, esti-
mated by the amount of innervation that we have given the
muscles. I say " we judge," but there is no conscious
judgment ; the estimation is by nerve-processes of which we
are imaware. If we want to touch this second object, we
adjust, also imconsciously, the degree of contraction of the
muscles of the arm, so as to enable us to effect the required
movement with instant precision. But if the eye muscle
concerned is weak, the increased innervation necessary for the
movement gives an impression of a greater movement than
has really taken place, and therefore an impression that the
object looked at is farther on that side than it really is, and if
the patient attempts to touch the object, his hand goes beyond
it. His ann moves, in accordance with the innervation of the
weak muscle, too far in the direction of the action of this muscle,
just as the other eye moved too far in the secondary direction.
Indeed, the erroneous direction of the arm corresponds exactly
with the direction of the secondarily-deviating eye. But the
knowledge of the relation of external objects to the body,
gained from the innervation of the eye muscles when we look
at the objects, is one of the most important guides to the centres
that regulate the maintenance of equilibrium. The erroneous
projection of the field of vision causes a discord between this
and other guiding sensations, and one effect of this discord
is the sensation that we call vertigo or giddiness. This

giddiness, depending on pamlysiB of an ocular muscle, is
termed " ocvdar vertigo, " and, lite other forms of vertigo,
is apt to cause mistakes in diagnosis. Tke nerve-centres,
after a time, learn to accommodate their action to the altered
oiroumatances, and both tlie erroneous projection and the
consequent vertigo cease to trouble the patient. When it
exists, the patient may try to avoid it Ly holding his head in
such a position as not to call the affected muscle into action,
and this will often put you at once upon the track of the
afEection. Or he may keep the affected eye closed, by conti'act-
ing the orbicularis. He always closes the affected eye, be-
cause, although dosing either eye would remove the diplopia,
only closure of the affected eye removes the vertigo or un-
certainty. He may thus show you which eye is at fault,
when 3'ou might find it difficult to asi'ertain. If you culti-
vate the habit of observing every point, however trifling it
may seem, you may often learn much of the nature of a
patient's ailment before he has got half-way across your

I may briefly summarize for you the chief symptoms of
the paralysis of each mxiscle. I will not ask you to try to
remember them now, but it may be convenient to you to have
the stmmiary for future reference. We will take, as examples,
the muficles of the right side,

S(lc(/i Nerve. — External Reetm. — Defect of outward move-
ment, convergent strabismus on looking to the right, with
simple diplopia, the two images parallel and on the some
level in the horizontal outward movement, but the false
image often on a difierent level, and obhque, when the eyes
ore directed above or below the horizontal level. Secondary
deviation of sound eye inwards. The head is held inclined
to the right,

Uiird Nerve. — Iidenial Reetm. — Defect of movement in-
wards, i.e., on looking to the left, with divergent strabismus,
and crossed diplopia, the false image oblique above and below
the horizontal plane. The head is inclined to the left.

Superior Rectus. — Defect of movement upwards, and espe-

J

OCULAR NERVES. 87

cially upwards and outwards; the inferior oblique, which
habitually acts with the superior rectus, being capable of
aiding the upward and inward movement, it may visibly
rotate the globe in so doing. Secondary deviation is by
the opposite superior rectus moving the eyeball too much
upwards. Diplopia occurs on looking upwards; the false
image is above the other, and the difference in level is
greatest in trying to look upwards and to the right.

Inferior Hectm. — ^Defect of movement downwards, and
especially downwards and outwards (because the downward
and inward movement is aided by the superior oblique) . There
is corresponding double vision, which is crossed. The false
image is below the others, and the lower the greater the
attempted movement; it is also oblique, especially on the
inward movement, from the rotation effected by the superior
oblique. Secondary deviation is by the opposite inferior
rectus.

Itiferior Oblique, — Defect of movement upwards, in which
position the muscle is an elevator (just as the superior oblique,
in the inward and downward movement, is a depressor). The
secondary deviation is also upwards and inwards, by the
inferior oblique and the internal rectus of the sound eye.
Double vision exists in the same movepient ; the false image
is above the other, and oblique, the obliquity being greatest
in looking outwards, the difference in height greater in look-
ing inwards.

Fourth Nerve, — Superior Oblique, — Defect of movement,
chiefly downwards and inwards, since in this position the
muscle is a depressor. Convergent strabismus exists in looking
down, and the corresponding diplopia is simple, the false
image being the lower, especially in an inward movement,
and oblique, especially in the outward movement ; the lateral
distance between the two is greatest in the middle line, and
lessens when the object is moved inwards or outwards.. The
diplopia, occurring on looking downwards, often gives the
patient much trouble in going down a flight of stairs, which
seems to be double, and he does not know which flight to
choose.

OB LECTirRE Vll.

You must not imagine, however, that it is always posdble
to determine with exactness the muscles that are affected iu the
derangement that results from brain disease. It is generally
possible when the ner\'es themselves are diseased, but in
oeutTal affections there is often a complex association of palsy
and spasm that may baffle all attempts to unravel it. I
remember, some years ago, one of the most distingiushed
ophthalmic surgeons in Europe, who knew, perhaps, more of
ocular palsies thou any one at that time H^-ing, visited the
Uueen Square Hospital and examined some patients for us.
After spending some time in the investigation of the defect
of movement of the eyes in one case, he said : " I can tell you
many things that it is not, but I cannot tell you what it is."

The special symptoms of paralysis of each ocular nerve need
not detain us long, since those of the sixth and fom-th nerves
are the palsies of the muscles they supply, the external rectus
and superior oblique. When the whole third nerve is paralysed
all the muscles are affected except the two just named; the
eyeball cannot be moved upwards or inwards, and only
shghtly downwards, while the unopposed action of the external
rectus usually causes the eye to de^-iate outwards. There are,
however, three other sjTnptoms : the upper hd droops from
the paralysis of the levator (ptosis) ; from the paralysis of
the sphincter of the iris, the pupil is midway between con-
traction and dilatation, and does not contract to Hght ; while
the paralysis of the cihary muscle aboUshes the power of
accommodation.

Isolated paralysis of these muscles is usually due to disease of
the nerves in the pons, in the crua, at the base of the brain, in
the orbital fissure, or in the orbit ; but curious associated palsies
are sometimes met with in central disease. Loss of the
upward or downward movements and of convergence {without
loss of other action of the internal recti) has been observed, and
is probably due to a lesion in or near the third nerve-nuclei
or in the corpora ijuadrigemina, usually degenerative in cha-
racter. Loss of the movement of both eyes to one side occurs
in focal lesions of the brain, and has been already mentioned

OCULAR NERVES. 89

(p. 53). I will only now tell you further that this "conjugate
deviation," as it is termed, may be the result of either
paralysis or spasm. In disease of the hemisphere the eyes
deviate in paralysis towards, £md in spasm from, the side of the
brain afEected. But in disease of one side of the pons they
may deviate in palsy from the side of the lesion. Sometimes
first one and then another ocular muscle becomes paralysed
imtil all have lost power, and the eyes are motionliBss, with a
peculiar imchanging stare. There may also be ptosis. This
affection — ^the progressive ophthalmoplegia of v. Graefe, the
ophthalmoplegia externa of Hutchinson — depends on a de-
generation of the nuclei of the muscles, analogous to that
which, in the cord, causes progressive muscular atrophy in
the limbs, and in the medulla oblongata gives rise to what is
termed " progressive labio-glossal paralysis."

The muscular mechanisms within the eye are susceptible
of four forms of paralysis. First, the ciliary muscle may be
paralysed, causing loss of accommodation, so that objects
cannot be seen well, except at a distance, and small print, that
could only be read near, cannot be read at all. The contraction
of the iris associated with accommodation may be lost, either
alone or with accommodation. The reflex contraction of the
iris, on exposure to light, may be lost alone, and so also may
the reflex dilatation on stimulation of the skin. Combinations
of these palsies often occur, especially of the associated action
of the pupil and of the ciliary muscle, and of the light and
skin reflexes. Loss of acconunodation may also be combined
with loss of convergence. Sometimes all the internal muscles
axe paralysed — ^the ophthalmoplegia interna of Hutchinson.
These internal palsies are rarely the result of focal lesions.
They result from influences acting on the nerve-elements
according to their function. Thus, in diphtheritic paralysis
the ciliary muscle especially suffers. Apart from diphtheria
the chief cause of these affections is degeneration, usually
associated with signs of degeneration elsewhere. This is their
chief diagnostic indication, and a very important one it is.

90 LECTirRK ^■II,

ParalyBis of the fifth nerve may involve the sensory or
the motor parts, or both. The symptom of the former is
anEBsthesia of the skin from the vertex to the lower jaw, and
of the mucous membrane of the nose, tongue, and mouth on
that side. Ammonia and snuiE no longer irritate the nasal
membrane, but odours can he perceived, although, after a
time, the sense of smell is blunted from defective secretion.
When the patient drinks, the cup, felt only on one side,
seems broken. Food is not chewed on the affected side
because it cannot he felt, and often because the muscles of
mastication are also paralysed : hence fur accumulates on that
half of the tongue, as it does whenever food cannot he chewed
on one side. There is much discrepancy of e^ddence as to the
influence on sensation at the back of the tongue and palate.
In some cases of disease limited to the root of the fifth nerve
there is ansesthesia of these parts, including the soft palate
and anterior palatine arch. In other eases these parts have
been sensitive. We do not know whether the difference de-
pends on personal vanations or on the position of the disease :
probably on the latter. Similar discrepancies exist with
regard to the affection of taste, as I have already told you
(see p. 25). Taste is usually lost on the front of the tongue,
and is certainly sometimes lost everywhere, even on the
palate and its anterior arch. The probable explanation of
this I have already given you. Trophic changes may result
from paralysis of the sensory part of the fifth. Of these
the most important is that in the eye. The cornea becomes
cloudy, then opaque ; ulcers form upon it, and may perforate,
and lead to a {iestnictive inflammation of the globe. Tliis
" n euro-paralytic ophthalmia," as it has been termed, probably
depends on the irritation of the nerve by the lesion rather
than on the anaesthesia or on the mere loss of nerve-influence,
and the irritation seems to be most effective when it involves
the Gasserian gangUon or the fibres from the gangUon in the
nerve in front of it. The symptom is rare when the disease is
situated between the ganglion and the pons, and the lesion there
has to be more irritative in character to produce the effect.

Paralysis of the motor part of the nerve causes weakness of

OCULAR NERVES. 91

the masseter and temporal muscles, easily recognized if you
make the patient " bite hard " while your fingers are on the
muscles on each side. If the loss of power is slight, the
weaker muscle seems to contract a little after the other. The
paralysis of the external pterygoid causes a defect in the
lateral movement of the jaw ; this can be moved towards the
paralysed side, but not from it. When the lower jaw "is
depressed, it deviates towards the paralysed side, because, in
depression, the external pterygoids draw the condyle of the
jaw forwards ; and this movement, occurring only on the
unaffected side, causes a deviation. The movement of the hyoid
bone is not perceptibly impaired; and although the tensor
palati and tensor tympani are said to be supplied by the
fifth, they do not seem to suffer when the root is diseased,
and hence, perhaps, their fibres come ultimately from some
other source. After a time the paralysed muscles waste,
the temporal and zygomatic fossse become flattened, and
ultimately a little secondary shortening of the muscles may
limit, in slight degree, the downward movement of the jaw.

Paralysis of the face is the result of disease of the fibres
or nucleus of the facial nerve, or of the motor path between
the facial nucleus and the cortex. This, as we have seen,
lies to the inner side of the limb-path in the cms, and
in front of it in the internal capsule, occupying the angle at
the junction of the anterior and posterior parts of the capsule.
The loss of power is on the same side as a lesion of the
nerve-fibres, or of the nucleus in the pons; but, since the
upward path decussates just above the nucleus, a lesion of
the upper part of the pons, of the cms, or of the hemisphere,
causes paralysis of the face on the side opposite to the lesion.
There is another difference between the effect of disease
above the nucleus and that of or below the nucleus. In the
latter case all parts of the face are affected; the eye cannot
be closed, the forehead cannot be wrinkled, and the mouth
can neither be widened nor firmly closed, the one half of the
orbicularis being paralysed. Hence the patient cannot

k

whistle, and lie ennnot " pitff " out a candle, for wMcli com-
plete closure and sudden opening of the lips are requisite.
But in the case of a supra-nuclear lesion the upper port of
the ffwie is little affected, and the orbicularis is scarcely
weakened, the chief palsy being that of the zygomatiei and
elevators of the upper lip. The explanation of this has
been already given in the account of hemiplegia, of which
such palsy usually forms part. Another important difference
is presented by the electrical reaction. In nuclear, and infra-
nuclear disease, the nerve-fibres degenerate, and the nerve-
trunk, in severe cases, can no longer be stimulated by any
form of electricity. The muscles no longer respond to fara-
daism, since the intramuacular nerve-fibres, on which only
faradaism acta, are degenerated; but the muscular fibres still
contract to the more deliberate stimulus of a slowly interrupted
voltaic current, and even act to this with greater readiness than
in health. This is termed the reaction of degeneration. I
have explained its characters more fully in speaking of the
diagnosis of diseases of the spinal cord. In the complete
form of facial paralysis, the loss of muscular tone and action
produces a strange effect on the aspect of the patient. In
the young, in whom the elasticity of the skin largely moulds
the features, the paralysis is little noticeable at rest, but is
grotesquely obtrusive on any movement of the face, one side
of which may be stem and unbending, while the other is
convulsed with laughter. In the old, however, the skin is
inelastic, and is thrown into wrinkles by the contracture in
which the muscles stereotype the emotions they have habit-
ually expressed. When the muscles become toneless, the
wrinkles disappear, and the palsy reproduces the unseared
features of an earlier age. The contrast throws into such
relief the effect of age, that patients often refuse to believe
that the smoother half can be unnatural, and maintain that
the wrinkles are the morbid appearance. Indeed you can
never place reliance on the statements of patients or their
friends as to the side of the face that has been affected. The
paralysis of the zygomatiei on one side permits their fellows
on the other to draw tlie mouth over, and far over on emotional

FACIAL NERVE. 93

expression. This renders the error an easy one. I have often
heard a patient say that the unaffected half of the face " must
have been the side that was wrong, because the mouth was
drawn right up to the ear." Physicians in their turn are liable
to be misled in another way. In cases that do not recover
perfectly a curious contracture occurs, and voluntary move-
ments, while less in degree, spread too widely over the face,
so that the eye closes unduly in smiling, and the comer
of the mouth is drawn up when the eye is closed. This con-
tracture deepens the naso-labial furrow; the normal side of
the face may be the smoother of the two, and may be thought
to be the paralysed side, imtil the degree of movement is
observed. This contracture, in the young, causes a deformity
almost as serious as the earlier palsy, but in the old it has
a cosmetic influence, bringing back the natural furrows, and
rendering the face symmetrical. The conunon cause of com-
plete palsy is neuritis of the nerve just within the Fallopian
canal, or eax disease, damaging it in its course through the
temporal bone, and you would not think of an intracranial
cause (within the pons or at the base of the brain) unless
there were other symptoms of such disease. When the
nerve is affected at the lower part of the canal, the chorda
tympani often suffers, and taste is lost in the front of the
tongue. It is often said that in disease of the nerve higher
up, the palate is paralysed, but I doubt whether this is
true. For fifteen years I have been looking out for paralysis
of the palate in disease of the facial nerve, and I have
never seen it. I am inclined to think that the opinion is
due to a misinterpretation of the very common congenital
obliquity of the uvula, and inequality of the palate.

LECTURE VIII.

SYMPTOMS IN THE REGION OF THE CRANIAL NERVES {Cm-
Hn-ucd): AUDITORY; GLOSSO- PHARYNGEAL; i'NEUMOGAS-
TRIG; SPINAL ACCESSORY— PARALYSIS OF THE LARYNX
AND OF THE PALATE— HYPOGLOSSAL NERVE— COMBINED
PALSY OF THE liULBAR NERVES.

t

Q-ENTLEMEN, — We will to-day continue and complete our
study of the symptoniB that are due to disturbance of the
fimction of the cranial nerves. The auditory and bulbar
nerves remain for consideration. The term "bulbar" is a
convenient designation for those nerves that arise from the
medulla oblongata. You will remember that the auditory,
facial, and sixth arise at the level of the junction of the pons
and medulla, but the facial and sixth asoend to their nuclei.
That of the sixth is altogether, and that of the facial in great
part, above its surface attachment, while the auditory nuclei
are at the level of origin of the neri'e. The nerves below the
auditory, the glosso-pharyngeal, pneumogastric, accessory part
of the spinal accessory, and hypoglossal, arise from, and have
their nuclei within, the medulla oblongata, and are therefore
those included in the term "bulbar nerves."

Disturbances of function of the auditory nerve are oc-
casionally important eymptoma of brain disease, but they

AUDITORY NERVE. 95

axe 80 far more frequently due to derangement of the delicate
and complex organ of hearing that the presumption is always
in favour of an aural rather than of a cerebral cause. The
symptoms of disturbance are three — deafness, tinnitus,
vertigo. Deafness may be the result of impaired conduction
in the nerve, or of disease of its centre. Tinnitus auriimi, or
"noises in the ears," is due to irritation of the nerve or
its central or peripheral terminations. Vertigo results from
interference with the fibres that are distributed to the semi-
circular canals, and subserve, not hearing, but perception of
the position and movement of the head — ^the fibres that
Cyon calls the "space nerve" (an inapt designation, although
the only one that has been given to this important part of
the auditory nerve).

The deafness that is due to disease of the auditory nerve is
the same in character as that which is due to disease of the
labyrinth in which the nerve-fibres end, but it is sharply
distinguished from that due to impaired conduction through
the tympanic cavity (middle ear) or external meatus. The dis-
tinction is that the latter impairs hearing through the air, but
leaves imaffected the perception of sounds conducted through
the bones of the skull. The former alters both alike. One
mode of ascertaining this is with a tuning-fork, and the test
depends on the fact that the hearing through the air is normally
rather more acute than that through the bone. A vibrating
timing-fork is held in contact with some part of the skull,
say the parietal eminence. As soon as it ceases to be audible
it is removed from the skull, and held opposite the auditory
meatus. It should be still distinctly heard. If it is not,
there is impaired conduction through the meatus or middle
ear, and the former can readily be excluded by the speculum.
If the tuning-fork is still heard, any deafness must be of nerve
origin, Le.y due to disease of the auditory nerve or nerve-
endings in the labyrinth. The watch affords another test
that is of great practical importance, not merely on account of
its convenience, but because it is even more delicate than the
tuning-fork, since perception, through the bone, of the short
high-pitched sound of a watch is, for some reason, often

I

impaired out of all proportion to the loss to the tuning-fork.
The meatus should be closed by pressing the antitragus over
it, the watch held close to, but not touching, the zygoma,
and the patient asked if he can hear it. It should then
be pressed firmly on the zygoma. In health it can scarcely
be heard in the former position, but the sound becomes
loud as soon as it is pressed against the hone. This is
the case also in disease of the middle and external ear. In
disease of the labyrinth and nerve, it is common for the sound
t« be quite inaudible when the watch is in contact. When
this is the case we can be quite sure that there is nerve-
impairment. Indeed, a caution is necessary on account of
the delicacy of the teat. Many persons, especially after
middle life, have lost the power of hearing a watch through
the bone, when they are conscious of no impairment of ordi-
nary hearing. This is no doubt due to pathological changes
in the labyrinth, for the change is often one-sided, and many
of these persons suffer from tinnitus or vertigo. If the sound
is still heard through the bone, although not so loudly as in
health, we cannot infer disease of the labyrinth or nrare,
because simple anchylosis of the stapes will lessen perosseal
hearing {since some vibrations pass through the chain of hones) ,
but no disease of the middle ear ^vill extinguish all hearing
through the bone. Galton's whistle, by which a very high-
pitched note is produced, may also be used to test the hearing
of such continuous sounds, but the pathological significance
of their loss has yet to be defined. Very rarely a limitation
of hearing exists, analogotis to the limitation of the field of
vision. It probably occurs chiefly in degeneration of the
optic nerve. Thu^, a patient with locomotor ataxy and
optic nerve atrophy, who doubtless has also atrophy of
the auditory nerve, has gradually become considerably
deaf to all soimds, and is absolutely deaf to the loudest
musical notes above E of the treble clef, and below the
lower 6 of the bass.*

• Since the above waa written, tbe range of hearing has gradnallj become
further reatritted, until only the notas between the two E'b of the treble elef
can be perceived. Even the lower £ Hat ia inauiUhle.

AUDITORY NERVE. 97

Deafness from intracranial disease is usually due to disease
of the nerve at the base of the brain, less frequently of its
nucleus in the medulla. It very rarely results from disease
of the auditory centre in the first temporo-sphenoidal con-
volution, and is then on the side opposite to the disease.
Bilateral deafness may be due to damage to both auditory
nerves, and I have also known it to be produced by a
tumour of the corpora quadrigemina damaging the upper
layer of the tegmentum of each cms cerebri, in which
the auditory path lies. From symmetrical disease of the
cortical centres it is extremely rare. But deafness on both
sides is frequently due to symmetrical labyrinthine disease.

Subjective noise, tinnitus aurium, is, like deafness, usually
aural in origin. It may result from almost any disease in
any part of the ear. It may be due to an abnormal sensi-
tiveness to the movements that are normal in the ear — of the
blood in the vessels (especially in the internal carotid), or of
the muscles within the tjrmpanic cavity, — or it may be due
to an abnormal increase of these movements, e,g,^ to an in-
creased vibration of the moving blood in anaemia, or in carotid
aneurism. It may be due to pressure on the auditory nerve,
or to irritation, functional or organic, of the auditory centres.
Its characters are extremely varied. The first point to be
ascertained is whether the sound is pulsatory or continuous.
In the former case the pulsation will be found to be syn-
chronous with the heart's action, and the sound probably
has its origin in the ear. Such a soimd has been known
to be due to an aneurism, and to be audible on aus-
cultation of the skull. This is the only case in which a
murmur is so audible, and so the diagnostic significance of
the phenomenon is great, although it is extremely rare.
Sounds that are due to irritation of the labyrinth or nerve,
or are of central origin, are usually (though not always)
continuous, and not pulsating. The next important fact is the
elaboration of the soimd. Soimds that are of simple charac-
ter, "nmibling," "buzzing," "hissing," "whistling," may be
of either local or central origin, but those that are of higher
elaboration, such as bells or music, are generally, the latter

H

always, of oentral origin. I have known tlie sound of bells
ringing to be the aura of epileptiform convulsions due to a
tumour beneath the first temporal convolution. "We have
little definite knowledge of the relation of tinnitus to disease
of the auditory nuclei of the medulla, but the soimd of a
loud crash has attended the onset of acute lesions in the
vicinity of the nuclei. Whether the sound is referred to the
ears, or vaguely to the head, is of little diagnostic import-
ance. Intense bilateral sounds of subjective origin are
usually referred to the head, and not to the ears. Tinnitus
and deafness are often associated, and must then be ascribed
to the same cause. The vertigo that results from afEection of
the auditory nerve will be considered in connection with
other forms of vertigo.

The glosso-pharyngeal nerve and the pneumogastrie need
not detain us long, since their isolated afieotion forms a less
frequent factor in the diagnosis of brain disease than does a
general derangement of their function. This may occur from
a severe lesion in any part of the brain, but is most conspicu-
ous when the disease is in the medulla oblongata. We will
consider subsequently the chief symptoms that are due to
derangement of the visceral functions of the pneumogastrie,
and deal now only with two effects of the impairment of
these nerves — paralysis of the pharynx, and paralysis of
the larynx. With these, however, we may, for reasons
that will appear as we proceed, most fitly consider the
paralysis of the palate.

The motor ner\'e-supply to the phaiynx is derived from
the pharyngeal plexus, into which both the glosso-pharyngeal
aud jmeumogastrio ent«r largely, and we do not know from
which of these uer\'es the motor fibres come. In paralysis of
the pharynx, swallowing is difficult ; food is apt to lodge, or
get into the larynx, and particles may even find their way
into the lower air-passages, and, after a time, set up chronic
disease in the limg. Paralysis of the pharynx is rarely an
isolated symptom of brain disease, and its diagnosis is not

^

PHARYNX ^LARYNX. 99

difficult. I have known it to be mistaken for cancer, but an
examination should prevent the error. Palsy is painless,
while cancer rarely is, and the former is usually accompanied
by loss of power in adjacent parts.

You will remember that the larynx receives only sensory
fibres from the pneumogastric proper, its motor fibres coming
entirely from that part of the spinal accessory that joins the
vagus. You will remember also that the superior laryngeal
nerve contains the sensory fibres for the vocal cords, and for the
larynx above them, and motor fibres for the crico-thyroid
muscle, while the inferior or recurrent laryngeal supplies all
the other muscles that act on the glottis, and contains the
sensory fibres for the larynx below the vocal cords. The
vocal cords are abducted, and the glottis opened, chiefly by one
muscle — ^the posterior crico-thyroid — ^which passes upwards
and outwards from the back of the thyroid to the outer
muscular process of the arytenoid ; and, drawing this back,
moves the vocal process outwards. The cords are adducted,
and the glottis closed, by several muscles, of which the most
important is the lateral crico-arytenoid, which, passing back-
wards from the side of the cricoid cartilage to the outer process
of the arytenoid, moves this forwards, and is thus the opponent
of the posterior muscle. But the outer fibres of the thyroid-
arytenoid muscle, which pass, parallel to the vocal cord,
from the thyroid cartilage to the muscular process of the
arytenoid, have a similar although feebler action. This closing
rotation of the arytenoids is supplemented by the arytenoideus,
which, passing from the back of the one to the back of the
other arytenoid cartilage, brings the two together. The vocal
cords are lengthened and made tense by the crico-thyroid,
which draws back and slightly tilts the cricoid cartilage, and
they are made tense or lax in parts by the inner fibres of the
thyro-arytenoideus, which end at different points along the
cord. But the muscular mechanism must be much less simple
than this. In the case of some muscles, all the fibres have
not the same direction, and may have different actions accord-
ing to their association. Doubtless, in the delicate and varied

h2

K

actions that produce vocal soimde, complex associated aotioaB
of the fibres are concerned.

The symptoms of paralysis are threefold — altered phona-
tion, deranged regTilation of the entrance of air in breathing,
and defective movement (observable with the laryngoscope).
The phonic and respiratory functions of the glottis are sub-
served by the same muscles and the same nerves, but by
centres that must diif er in their anatomical connection, if they
do not in their anatomical position. After death, the vocal
cords are in a position of alight abduction from the middle
line, and this, termed the " cadaveric position," must be
regarded as that of muscular relaxation — of that rest which,
during Kfe, they never actually attain, since they move with
every breath. They move farther apart during inspiration;
they come nearer together during expiration; while in phona-
tion they are brought very near together aud made more tense.
In total paralysis of all the muscles, the cords are in the cada-
veric position, and do not move with breathing or on an attempt
to produce sotmds. Instead of the natural explosive cough
there is only a rush of air through the glottis. There is some
stridor on a forcible iEispiration. If only one vocal cord is
completely paralysed, some hoarse phonation may still be
possible by extreme adduction of the normal cord, and its
abduction prevents inspiratory stridor, hut a proper cough is
atill impossible. Such one-sided palsy may result from disease
of the nucleus of the spinal accessory in the medulla, of its
roots at the smiace of the medulla, of the trunk of the vagiia,
and even of the recurrent laryngeal, since the escape of the
orico-thjTxtid in the latter ease does not materially modify
the symptoms. Hence the palsy itself does not help us to
determine the position of its cause.

In other cases of bilateral palsy the cords are nearer toge-
ther than the cadaveric position. They can be approximated
for voice or cough, and when the effort is over, their elasticity
may make them recede a little ; but they cannot be abducted
even as far as the cadaveric; posture, and the normal separation
during inspiration does not occiu-. This is called pai'alysis of
the abductors, the posterior crico-arytenoids. The li

1 pai'aiysis oi i

he longer the J

LARYNGEAL PALSY. 101

palsy lasts, the closer together are the cords, in consequence
of a secondary contracture of the unopposed adductors. The
cords being always in the position of phonation, voice is little
affected, but the absence of the normal separation during inspira-
tion causes a serious impediment to respiration, since the inrush-
ing air brings the cords still nearer together, and causes a loud
inspiratory stridor, and dyspnoea on the least exertion. The
absence of expiratory stridor distinguishes the dyspnoea from
that due to tracheal stenosis, and, together with the integrity of
the voice, distinguishes this from any other laryngeal affection.
The condition is one of considerable danger, since the least
catarrhal swelling of the mucous membrane may necessitate
immediate tracheotomy to prevent suffocation. K this abductor
palsy is one-sided, the symptoms are slight or absent, and the
diagnosis can be made only by the laryngoscope. The most
frequent cause of abductor palsy is central degeneration ; but it
sometimes occurs, strange to say, in severe hysteria, even, as I
have seen, in extreme degree. Equally strange is the well-
established fact that it may result from disease of the recurrent
laryngeal, which, supplying the adductors also, should cause
only a total palsy. This has given rise to much speculation as
to its mechanism. Some light seems to be thrown on it by
the fact that electrical stimulation of the recurrent laryngeal
also causes adduction, although aU the muscles, adductors and
abductors, must be equally stimulated to over-action. This
must be due to the greater power of the adductors, perhaps
also to the mechanical advantage at which the chief adductor,
the lateral crico-arytenoid, acts, in comparison with the ab-
ductor, the posterior crico-arytenoid, since the former passes
nearly at right angles, the latter at a very acute angle, to the
muscular process of the arjrtenoid cartilage. A force acts on a
lever at greatest advantage when applied at right angles to the
lever. The effect of a general imder-action may be to impair
the effect of the abductors more than that of the adductors, just
as the general over-action on electrical stimulation increases
the effect of the adductors out of proportion to that of the
abductors. According to this explanation, the abductor palsy
would be the effect of paralysis of the recurrent, when it is

103

incomplete in degree, although not necessarily partial in dis-
tributioii ; while the total palsy with cadaveric posture would
he the result of complete paralysis. In harmony with this is
the fact that in progressive disease of the recmrent an initial
ahductor palsy has heen ohserved to pass into total palsy
{Scheeh, Rosenhach). In some cases, as Riegel suggests,
secondary contracture of the crico-thyroid may aid in causing
the adduction ; hut siaee adduction is often ahaent in total
recurrent palsy, the influence of this contracture cannot he

great. When the palsy
type, secondary tissue- changes
may perhaps maintain the g]
the palsy has become comph
In simple adductor palsy

and for long, of the ahductor
in the preponderating adductors
lottis in adduction, even when
ta

;he cords are apart, and cannot
he brought together, hut further abduction occurs in deep
inspiration. The cords are not approximated in speech, and
80 the patient is voiceless, hut they can still he brought
together in coughing. Hence it has heen termed by Tiirok,
"phonio paralysis."' This is the cause of hysterical aphonia,
but is scarcely ever produced by organic disease. It is readily
distinguished, by absolute voicelessness and perfect cough,
not only from other laryngeal palsies, but also from other
diseases, such oa catarrhal laryngitis, in which there is a
hoarse attempt at phonation.

These laryngeal palsies can be diagnosed with certainty
only by the aid of the laryngoscope; but the symptoms
themselves often Justify a strong suspicion of the nature of
the aifection, and it may he well to put them before you in
the form of a table. Tou will see that the inabihty to effect
an explosive cough is of great significance, and should lead
you to suspect a palsy, probably of organic origin ; you will
observe that if voice is also entirely lost, the palsy must be
double. If voice is preserved and cough lost, you suspect
ons-sided palsy. Loud inspiratory stridor with preserved
voice means double ahductor palsy ; a normal cough and no
voice or stridor signifies an unimportant adductor palsy.

* A much more eiact term than hia attractive liut Ii
tion of " respiratoiy paralysis " for aMuctor palsy.

LARYNGEAL PALSY.

103

SYMPTOMS.

SIGNS.

No voice ; no cough ; stridor
only on deep inspiration.

Voice low-pitched and
hoarse ; no cough ; stridor
absent or slight on deep
breathing.

Voice little changed ; cough
normal; inspiration difficult
and long, with loud stridor.

Symptoms inconclusive ;
little affection of voice or
cough.

No voice ; perfect cough ;
no stridor or dyspnoea.

Both cords moderately
abducted and motionless.

One cord moderately
abducted and motionless,
the other moving freely,
and even beyond the middle
line in phonation.

Both cords near together,
and during inspiration not
separated, but even drawn
nearer together.

One cord near the middle
line not moving during in-
spiration, the other normal.

Cords normal in position
and moving normally in
respiration, but not brought
together on an attempt at
phonation.

LESION.

Total bilateral
palsy.

Total unila-
teral palsy.

Total abductor
palsy.

Unilateral ab-
ductor palsy.

Adductor
palsy.

The nerve-supply to the palate is one of those points in
anatomy that urgently require re-investigation. The most
important muscle is the levator palati, which receives a nerve
from the spheno-palatine ganglion, hut the ultimate origin
of its fibres is certainly not from the fifth nerve. They are
usually said to come by the Vidian from the facial, but they
probably reaUy come from one of the bulbar nerves, either the
glosso-pharyngeal or spinal accessory. Paralysis of the palate
results from disease of these bulbar nerves (at the surface of
the medulla) or of the bulbar nuclei. It is doubtful whether
it ever results from disease of the facial nerve, and certainly it
does not from disease of the fifth. The centres for the palatine
muscles are especially obnoxious to the mysterious influence
that diphtheria leaves behind it, and this is the most frequent
cause of simple palsy of the palate. In total palsy, the soft
palate hangs low and flaccid, the uvula is long, and no move-
ment occurs in drawing a deep breath, in phonation, or on
tickling the mucous membrane. The posterior nares are no
longer closed. Hence, during swallowing, liquids are apt to
come back through the nose; during speaMng there is a
nasal resonance, and the explosive consonants, as p and ft, are
no longer properly articulated, because the patency of the nares
prevents the necessary compression of the air in the mouth,

w

and they are tranaf ormed into m. In unilateral paJsy these
symptoms are abeeut. All the muscles, even of one side, are
rarely paralysed, since unilateral palsy is scarcely ever due to
disease of tie centre (which affects both sides), and the oourae
of the fibres to the different muscles is not the same, and
therefoi-e a lesion does not affect all of them. The palate at
rest presents little change iu unilateral paralysis. On one
side it may be a little lower than the other. The uvula may
hang a little to one side, but palsy never causes any curve
iu the u^Tila, and no abnomial position of the palate or
uvula cau be due to paralysis, unless it is increased on move-
ment. The moat important symptom of one-sided palsy is
recognized only on movement. At rest, the palate may
appeal' equal, but if the patient is made to say "ah," the
base of the uvula deviates a little to the unaffected side, and
a little on this side of the middle line, about midway between
the arch and the hard palate, a slight dimple forms, while
the unparalysed side remains smooth. The difference is
obvious and characteristic. There is no deviation of the nvida.
The difference between the two sides, on movement, evidently
depends on paralysis of the levator palati. It occurs together
with paralysis of the tongue and vooal cord on the same side,
when there is disease at the side of the medulla damaging
the hypoglossal and spinal iweessory nerves. This was first
pointed out by Dr. Hughlings- Jackson. Whether the para-
lysis depends on the disease of the spinal accessory, or on
disease of the adjacent glosso-pharyngeal, is uncertain, but
the association leaves no doubt that the motor fibres for this,
the most important of the palatine muscles, come from one of
these bulbar nerves. I have known the same three palsies
(tongue, palate, and vocal cord) to result from a deep-seated
tumour in the upper part of the neck, which must have
damaged the nerves outside the skull.

"When the accessory part of the spinal accessory is injured
by disease at the foramen magnum, the spinal portion may
suffer also, causing wasting and loss of power of the stemo-
mastoid and upper part of the trapezius.

BULBAR PALSY. 105

Disease of the hypoglossal nerve, outside or within the
medulla, causes paralysis of the same half of the tongue ;
and disease of the motor tract above the nucleus causes
paralysis of the opposite half of the tongue. Disease of the
nucleus itself almost always causes paralysis of both sides of
the tongue, because degeneration affects both nuclei, and the
two lie so near together that both suffer in acute lesions.
In one-sided palsy, the tongue, at rest, is in its normal
position in the mouth, but the base is higher on the paralysed
side, owing to lack of tone in the posterior fibres of the
hyoglossus. Within the mouth, movement is deficient
towards the paralysed side, but on protrusion the tongue
deviates from the sound, and towards the paralysed side, being
pushed out and over by the imaffected genio-hyoglossus. In
bilateral palsy the tongue lies motionless within the mouth,
and cannot be moved. In disease of the nerve or nucleus,
the tongue usually wastes, and the mucous membrane lies in
irregular folds over its surface.

The process of articulation is effected by the muscles sup-
plied by these bulbar nerves, and its impairment always con-
stitutes an important sjrmptom of their disease, or of disease
in the part of the brain from which they arise, and in which
a complex structural association subserves the conjoined action
of the various muscles concerned in the process. Articulation
consists in stopping and varying the outgoing current of air,
which is often thrown into vocal vibrations, on which the pro-
cess of articulation effects more elaborate and perfect modula-
tions than it can in merely whispered utterance. In the
whole series of movements that can be effected by the muscles
of man, there are none comparable to these in exquisite
delicacy of adjustment, and in the infinite diversity of result
that a few simple muscles can produce by their combined
action. It is not surprising that commencing failure of the
adjustment of nervous action should be manifested in these
sooner and more than in any other mechanism. There are
two chief forms of defect of articulation. The first is due to
paralysis of the muscles, and in this the loss of power can

106

I.ECITRE VIII.

w

1)6 recognized in other movements. The precise form of
defect depends on the musdes that are weak, and this I have
ab-eady alluded to, and will return to in a moment in speak-
ing of the combined palsy. In the other variety there is
no actual paralysis, but the delicate adjustment is at fault.
Syllables are run together, in what may be termed " con-
fluence of articulation " ; the ends of words are not well
pronoimoed, are even elided; or the syllables may be un-
duly separated, in what is termed, from a musical analogy,
" staccato " utterance. The most delicate of all the move-
ments is that involved in the pronunciation of )■, and it is
in this that the commencing defect is often most conspicuous,
as by making the patient say "truly rural." Often there is
a peculiar drawl, and this may be combined with eUsion of
syllables. In many cases, and especially in the paralytic
defect, the patient can utter a word by a deHberate effort
much better than he does in habitual speech.

Before leaving the subject of the symptoms of the cranial
nerves, one other subject should be noticed. Certain of these
nerves are liable to suffer together from disease of their
nuclei, usually from degenerative disease. The nerves thus
associated in disease are the two groups of motor nerves that
are associftted in function. The first group is that of the
nerves for the eyeball muscles, and its disease causes the
progressive ophthahnoplegia that I have already mentioned.
The other group is that of the nerves for the complex series
of muscles of the orifice and upper part of the respiratory
passages, mouth, throat, and larynx, — the fibres of the facial
for' the orbicularis oris, the hypoglossal, the fibres to the
palate, perhaps from the glosso-pharyngeal, those that give
motor power to the pharynx, and the laryngeal fibres of
the spinal accessory. Before considering the associated palsy
that results from nuclear degeneration, I may remind you of
the associated one-sided palay of tongue, palate, and larynx,
■which I have just described as the result of disease outside
the medulla. The tongue deviates to one side ; the middle
of the soft palate is drawn to one side when it is raised, and

BULBAR PALSY. 107

if the laiynx is examined, the vocal cord on that side is seen
to be motionless. These symptoms are due to damage to the
roots of the hypoglossal, spinal accessory, and perhaps also of
the glosso-pharyngeal.

In the associated nuclear palsy — " bulbar paralysis," as it is
often teTMsd-th, i»»lyi ta'olv,, th, ^e ^ U^.
palate, and vocal cord ; but it is bilateral, and its functional
distribution is more complete, since the lips and pharynx are
usually also involved. You will remember what I said of the
central relations of the nerve-fibres.for the lips : although they
run in the facial nerve, they must be derived from nerve-cells
that have the most intimate connection with those for the
twinsverse muscle of the tongue, and the two may even be de-
rived from the same nucleus. The association of the lips with
the other parts caused Duchenne to give to the disease the
name "labio-glosso-pharyngeal paralysis," by which it is still
often known. The symptoms are, as it were, grouped about the
tongue as a centre, and it is in the delicate movements of lin-
gual articulation that the first symptoms occur — a climisiness
in the pronimciation of the lingual consonants /, r, n, ^, and s.
Subsequently the degree of protrusion of the tongue becomes
impaired, imtil at last only the tip can be put beyond the teeth.
It is often conspicuously wasted. The early weakness of the
hps prevents whistling, and the labial explosives b and p
become/, and v becomes u. This transformation is assisted
by the weakness of the palate, which ceases to shut off the
nasal cavity, and so interferes with the compression necessary
for explosive sounds; hence also nasal resonance persists in
all sounds. Swallowing becomes difficult ; liquids regurgitate
into the nose ; food gets into the larynx, and this may be so
paralysed that the glottis cannot be closed, and an explo-
sive cough is impossible. Ultimately a low, hoarse vocal
sound is all that remains of speech; but it is rare for the
paralysis of the larynx to be complete.

SYMPTOMS {Continued): MENTAL DISTURBANCE— LOSS OF CON-
SCIOUSNESS— APOPLEXY— DELIRIUM— MENTAL WEAKNESS
—LOSS OF MEMORY.

¥

Gentlemen, — ^The Bymptniiis that have hitherto engaged
our attention are the derangementB of special funotioua
suhserved by special nervous structures. Those that we
have now to consider are more general in natiire, and the
symptoms caused by their derangement axe for the most
part "diffuse." It is convenient to consider with these
some symptoms that are "fooal," hut which are closely
allied to those that are general. Thus it is better to study
defect of speech, a focal symptom, after we have considered
derangement of mind, a general symptom.

The highest functions of the brain are those concerned
in mental processes, and the derangement of these is a
frequent and obtrusive effect of organic brain-disease. But
these symptoms do not stand in the special and pre-eminent
relation to such disease that might reasonably be anticipated.
The highest cerebral fimctions are so readily disturbed, that
their derangement is less frequently the result of organic
brain-disease than of changes in the blood, on the one hand,
or of the minute altarati^ms of nutrition that we term func-
tional disease, on the other hand. The most significant dis-
tnrhance from organic disease is the coarsest, such as unoon-

LOSS OF CONSCIOUSNESS. 109

sciousness. The slighter disturbance, such as delirium,
derives its significance from its associations, not from its
simple presence.

We may consider first the profoimd and important mental
symptom that I have just mentioned — ^loss of consciousness.
Remember that the terms " conscious" and " consciousness "
are used in two senses : first, to signify subjective knowledge
of the occurrence of mental processes ; and secondly, outward
manifestation of such processes. In medical language the
words are chiefly used in the second of these two senses.
A patient is said to be " unconscious," or to have " lost
consciousness," when there is no evidence of mental action,
either spontaneous or in response to attempts to elicit it.
The term " insensible " is often applied to the same condi-
tion. Another confusion is introduced by the use of the
term " conscious of," or " unconscious of," in the sense of
cognition, or its absence. Thus a delirious patient is said to
be imconscious of what is occurring around him, although
he is not said to be imconscious.

Loss of consciousness may occur suddenly or gradually,
may be complete or incomplete. The variations may be in
the degree of subjective consciousness, or of the external
manifestation of consciousness ; and it is to the latter that the
term " partial loss " is usually applied, as, for instance, to
the condition in which a patient lies apparently asleep, but
opens his eyes when spoken to, immediately relapsing into
sleep. This condition is often termed " stupor." Complete
unconsciousness, lasting more than a few minutes, is termed
"coma." In both conditions there is usually imperfect
control over the sphincters. In stupor, the reflex action on
the limbs is preserved, and sometimes increased; the patient
swallows automatically liquid placed in his mouth; the
pupils act to light. In coma, the reflex action in the limbs is
usually lessened, and often lost. Muscular tone gives place to
flacddity, and with this change myotatic irritability often
disappears. The pupils may be widely dilated or small, and
do not act to light, at any rate when the coma is deep, and
then the conjunctival reflex is also lost. The act of swallow-

110 . LECTUKE IX.

ing may or may not be poBsible ; in deep coma it is lost,
and the palate, eharing tlie muaoular relaxation, vibrates
under the current of air, and causes the peonliar " stertor "
which is a familiar indication of the depth of coma. Even
the respiratory movements are lessened, in consequence of
lowered activity of the respiratory centre; they become
shallow, infrequent, and sometimes present rhythmical
variations of intensity, in what is termed the " Cheyne-
Stotes breathing" — alternating periods of decreasing and
increasing depth of breathing, separated by a pause. The
lessened breathing fails to clear the air-passages of the
secretion in them ; this accumulates in the bronchial tubes,
and ia often erroneously regarded as evidence of bronchitis ;
finally, mucus collects in the trachea, and causes the well-
known harbinger of death.

Consciousness may be impaired by almost any one of the
many morbid processes to which the brain is liable, whether
acute or chronic. It results from chronic and subacute
disease chiefly when this damages a considerable area of the
cortex, either directly, or indirectly by causing a rapid or ex-
treme increase in the intracranial pressure. It results from
sudden lesions in any part of the brain, and is then usually
sudden in onset, and termed " apoplexy."

Of all the sudden lesions that cause apoplexy, intracranial
hfemorrhage is the most effective, and the most frequent;
hence " apoplexy " has come to be a synonym for internal
hseraorrhftge, whatever be its seat. Next in frequency is the
sudden ocdnsion of a large artery by a ping brought from a
distance (embolism), or formed in situ (thrombosis). It may
result from congestion of the brain, although it does so far
less frequently than is commonly supposed. A similar sudden
loss of consciousness may occur in the old without any visible
lesion of the brain to which it can be ascribed. This has
been termed "simple apoplexy." In senihty the brain
shrinta ; the space between the convolutions is occupied by
serum. This change, which is common in the old, and
without significance, when found in old persons who had died
of simple apoplexy was thought to be important, and the

APOPLEXY. Ill

cause of death; hence the condition was termed "serous
apoplexy" — ^a disease that has no real existence, although
the name still survives, and now and then finds its way into
certificates of death.

The characteristic of apoplexy is sudden loss of conscious-
ness, not due to any cause outside the nervous system, such,
for instance, as failure of the heart's action or a poison in the
blood. The onset may be sudden ; the patient falls as if
" struck " down by some unseen hand, — ^an idea that is fos-
silized in the name, and in its EngUsh synonym, a " stroke."
Sometimes the onset is gradual ; consciousness slowly fades ;
stupor slowly deepens into coma : and this has been termed
"ingravescent apoplexy." The face may be flushed or pale;
it is rarely very pale. Often the heart and arteries pulsate
strongly, but sometimes less frequently than normal. The
temperature is usually at first depressed; its subsequent course
varies with the cause of the apoplexy. An exception to the
initial depression of temperature is presented by active lesions
of the pons, which, whatever be their nature, are sometimes
attended with a rapid rise of temperature, that may, in an
hour, reach 105° to 106°. If the attack is one of moderate
severity, reflex action soon returns, and in the course of a few
hours some indication of returning consciousness can be per-
ceived. On the other hand, the coma may deepen, and the
interference with breathing, already described, may come on.
In most cases the symptoms of apoplexy are accompanied by
those of a local cerebral lesion, commonly by those of hemi-
plegia, previously detailed.

The symptoms of apoplexy are those of lowered cerebral
function, beginning at the highest, and extending down-
wards to lower centres in proportion to the depth of the coma.
Its precise mechanism has been much discussed, but is a
matter of theoretical rather than of practical importance. It
is easy to frame a simple and satisfactory hypothesis of the
way it is produced by any one lesion, but the variety of its
causes shows that more than one mechanism may be concerned
in its production, and suggests that its origin is complex in
every case. Sudden increase of intracranial pressure causes

p

112 LECTURE IX,

loss of consciouBnees, but in what degree the result i
due to the mechanical action on the nerve-elements, or to
ansBmia from the compression of the capillaries, is uncertain.
This mechanism is doubtless effective in cerebral hemorrhage,
but it is probably not the sole mechanism, even in this case,
because apoplexy may result from a very small hremorrhage,
and consciousnesB may be lost at the very onset of a
hEemorrhage. The sudden occlusion of a vessel will cause
apoplexy, but cannot do so by its influence on the intra-
cramal pi'essure. Attempts that have been made thus to
explain it are remarkable chiefly for their ingenuity.
In moat cases of apoplexy there is a sudden damage to
nerebral tissue. Sudden arrest of blood-supply constitutes
a damage as effeotiuil as laceration. Hence it is probable
that one element in the production of the loss of con-
sciousness is the inhibitory effect of the irritation of the
lesion. We have evidence of a downward influence of this
character in the initial loss of muscular tone and muscle reflex
action {e.g., in the loss of the knee-jerk*). A similar upward
action, inhibiting the highest centres, is probably the cause of
the initial loss of consciousness, the prolongation of which may
be helped by other meehanieras, such as increased pressure.
All lesions are effective in proportion to the rapidity with
which they are produced. Experiments, for iustance, show
that the amount of intracranial pressure needed to abolish
consciousness has to be ten times greater when slowly than
when rapidly produced.

The diagnosis of the cause of apoplexy we shall consider
when we come to the last part of our subject — to the indi-
cations of the nature of the brain disease, — but I may briefly
point out to you seme of the chief differences between the
coma of cerebral origin and that which may result from causes
outside the nervous system, or from cerebral derangement
that is merely functional in character. In all cases the most
important point is to search carefully for any evidence of a
local cerebral lesion, and especially for the indications by
' See " DiagnosiH of Diseases of the Spinal Cord," 3cd Ed., p. 31.

APOPLEXY. 113

which hemiplegia can be recognized during the state of coma.
These I have already described to you (p. 54). The reflex
actions are of especial importance. If these are all perfectly
normal, this is, in the absence of other decided symptoms,
against the existence of a cerebral lesion. An abnormal
condition of reflex action is in favour of it, and is almost con-
clusive if the abnormality is unilateral.

We will take first the functional disorders of the nervous
system. A patient may be unconscious for an hour or
two after an epileptic fit, and this may be mistaken for
apoplexy with a convulsion at the onset. Such a diffi-
culty can scarcely arise unless the history of the patient
is unknown, since first convulsions are rare, except in those
in whom cerebral apoplexy is also rare. Post-epileptic
unconsciousness resembles sleep more than it resembles
coma. The patient can be readily roused. The temperature
is nearly normal — ^never below normal, as. it often is in
apoplexy, — and unilateral symptoms are absent,. The con-
vulsions that cause transient post-epileptic hemiplegia are
always one-sided, and are not followed by such deep sleep
as to raise the question of a possible cerebral lesion. The
patient soon emerges from the mental obscurity that
follows an epileptic fit, and often at once passes into a
normal condition, but occasionally is still " befogged "
for a longer or shorter time — ^in a wandering, stupid state
of mind, that is itself very characteristic.

The state of unconsciousness that occurs in rare cases of
hysteria simulates apoplexy less than it resembles the coma
due to less rapid cerebral processes, such as meningitis. A
patient, for instance, after a period of headache, becomes
unconscious, swallows what is put in the mouth, but cannot
be roused. The diagnostic indications are the age and sex
of the patient, who is usually either a female or a boy ; the
absence of any cause of a cerebral lesion; the history of other
symptoms of functional nervous disturbance (especially of
hysterical convulsions or vertical headache) ; the cessation
of headache when the coma comes on; the absence of all
objective symptoms; the inconsistence between the ready

p

114 LKCTUHE IX.

deglutition and the apparent deptli of coma; and the
miiform course of the affection, which often presents no
change for many days.

Of causes outside the nervous system, urtemio poisoning
is that whicJi most often causes perplexity, hecause its
frequent cause, chronic kidney-disease in the second half
of life, is also a frequent cau^e of the apoplexy that it
resembles. Alhuminuria is constant in urEemia, frequent in
apoplexy ; its absence is therefore more significant than its
presence. In many eases the coma is preceded by other
ursemic symptoms, especially by convulsions or amaurosis.
Severe general convulsions may, it is true, usher in both
afEecfdons, but at the onset of apoplexy the convulsion is
usually single ; at that of urtemie coma there are many.
Sudden complete amaurosis is almost conclusive evidence of
uragmia. An acute cerebral lesion scarcely ever caiises total
blindness. Elevation of temperature is strongly in favoiu'
of cerebral mischief ; depression is consistent with either, but
oontinuouB depression, lasting for two or three days, is strongly
in favour of UKemia. An examination of the fundus of the
eye vrill, of course, be one of the first steps you take.
Albuminuric retinitis often proves the existence of renal
disease, when an examination of the urine is, for the time,
impracticable. It shows, moreover, profound systemic mis-
chief. It always indicates that the patient is in a state in
which ursemic symptoms may come.on at any moment. The
absence of retinal change does not exclude mremia, any
more than its presence proves that unemia is the cause of
the coma.

In profound aleohnlic poisoning the diagnosis from
cerebral apoplexy may be extremely difficult. When you
have no history to guide you, as is often the case witli the
patients who are brought to a hospital or a pohce -station,
the diagnosis may be impossible. Many a patient with
apoplexy has been locked up in a police-cell all night as dead-
drunk. Brandy is the universal panacea for impairment
of consciousness; and so apoplectic patients often smell of
alcohol. If focal symptoms are absent there is no distinctive

DELIRIUM. 115

indication. A few hours will always decide the question ; and
it is better to let a drunken man get sober in bed, than to let
a patient with ventricular hoemorrhage die in a police-cell.
We need, however, more facts regarding the state of reflex
action in profoimd alcoholic poisoning, especially of the
muscle reflex action (knee-jerk, foot-clonus, etc.). It is not
improbable that some useful guidance may be foimd in
these symptoms. This is one of the many points on which
those of you who are hospital residents may make valuable
observations.

The danger of confusing opium-poisoning and apoplexy
is not great, because the patient who has taken opium usually
comes under observation while the pupils are contracted to
an extreme degree — conclusive, except as regards the dis-
tinction from haemorrhage into the pons. In the latter
there is often a history of sudden onset, and usually
objective symptoms are present that permit no doubt as to
the nature of the case.

From the lessened manifestation of mental activity we may
pass to the disorder and excess that constitute " delirium," the
condition in which mental processes are not in accordance with
sense-impressions, and there is no consciousness of the dis-
crepancy. The condition is essentially the same as that which
constitutes " insanity" ; but the term delirium is used when
the mental derangement is acute in course, and occurs in
consequence of organic brain-disease or of some blood-state.
Delirium is commonly distinguished as " quiet " or " active."
In the former there are hallucinations, especially of sight,
and these dominate the patient's ideas. He often talks con-
tinuously, but in a low monotonous voice, and it may be
difficult to make out what is said — a condition aptly termed
"low muttering delirium." On the other hand, in "active
delirium " there is more energy in the manifestation of the
mental processes, and the patient tries to act according to his
erroneous ideas. Although the elements of delirium are
identical in nature with those of what is termed insanity,

certain common features of the latter rarely occur in delirium.

1 2

116 LECTURE IX.

Such are the extreme and persistent emotional depression
of melancholia, the exaggeration of idea that is common in
general paralysis of the insane, the outrageous delusions of
personal identity met with in some cases of chronic insanity,
and the rhetorical loquacity of acute mania.

Deliriimi is far less frequently the result of organic dis-
ease of the brain than of altered conditions of the blood,
especially that in pyrexia. There is rarely anything in the
character of the delirium to indicate to what cause it is due.
In acute alcoholic delirium, unpleasant visual hallucinations
are a marked feature, and there is usually conspicuous
tremor ; but chronic alcoholic deliriimi may present none of
these characteristics. The delirium due to pyrexia and that
resulting from organic brain-disease present no difference.
Since pyrexia is by far the most common cause of delirium,
this symptom alone is suggestive of organic brain-disease only
when there is no pyrexia, or only a slight degree of pyrexia,
insufficient to account for it. It must, moreover, be remem-
bered that those who are addicted to alcohol, and those who
are old, are rendered delirious by a slighter degree of blood-
change than is necessary in the case of the sober and the
non-senile. The caution to attribute no weight to delirium,
unaccompanied by other symptoms of brain disease, if the
patient has considerable fever, may seem a simple rule;
but, like many other simple rules in diagnosis, it is
often forgotten, and consequent mistakes are frequent.
Not long ago I saw a man who was said to have
inflammation of the brain, and I found he had only
inflammation of the lungs. The delirium had so misled
the doctor in attendance that he had not even examined the
lungs. Again, a child became feverish and delirious: the
medical attendant diagnosed tubercular meningitis, and
foretold a speedy death. But the pyrexia was sufficient in
degree to account for the delirium : there was no evidence of
anything more than a catarrhal f ebricula, and in a week the
child was well. Do not, however, go to the other extreme, as
some have done, and conceive that delirium is of no signi-
ficance as an indication of organic disease. It is significant

MENTAL FAILURE. 117

when there is no other discoverable cause, and it may both
confer and receive significance by association with other
cerebral symptoms. These may be various in character, but
one of the most frequent is headache. Headache, like
delirium, is an effect of fever. But the headache of fever
ceases when the delirium comes on; that of brain disease
persists. The coexistence and the sequence of the two have,
therefore, quite a different significance. If the patient is
delirious, and has, at the same time, severe pain in the head,
you should suspect organic disease. Of course, pyrexia often
accompanies delirium from organic disease, and we have then
to depend on the other symptoms for our diagnosis, or on the
order of the two. If the delirium precedes the fever, it has
evidently the same significance as if it existed alone. The
various other symptoms that may give significance to delirium
need not be enumerated here.

Mental weakness shows itself in failure of power in aU the
various mental processes, and of these loss of memory (" am-
nesia ") is the most conspicuous and the most tangible. Memory,
like other mental actions, has its physical side. Every func-
tional state of the nerve-elements leaves behind it a change
in their nutrition, a residual state, in consequence of which
the same functional action occurs more readily than before ;
and this residual disposition is increased by repetition. This
is the basis of motor training, which consists in a sort of
motor memory that enters little into the region of con-
sciousness. The same residual disposition in the cells that
act during mental processes no doubt infiuences the revival
of those processes in memory properly so-called. The
sequence of action of groups of nerve-cells is the physio-
logical aspect of that which, in its psychological aspect, we
term the association of ideas. There is no special faculty
of memory, physical or psychical, apart from the general
cerebral and intellectual processes. But there is, or seems to
us to be, a peculiar power of the voluntary revival of these
processes— of the re-energizing of the residual tendencies, — a
faculty that is popularly termed "recollection."

118 LECTURE IX.

Any disease of the brain may affect memory, whether it
be coarse organic disease or finer degenerative processes.
Moreover, temporary malnutrition, as from acute disease, or
severe anaemia, may have the same effect. The defect may
be seen in the inability to retain new impressions, or in the
loss of those that are recent. As Eibot has put it, "the
new perishes, the old endures." Strange examples of this
are sometimes met with. I have seen a clergyman who
had lost all memory of the last twenty years of his life.
Those years had passed over him, leaving their marks
indelibly on his frame. They had been years of active
work, and at the end of them he had an illness. When he
recovered, all memory of those years had vanished. In rare
cases of the kind, memory has returned, and the lost time
comes back in the order from the past towards the present.

Another symptom of mental failure, with which, indeed,
loss of memory is closely associated, is deficient power of
attention, of excluding all but one subject from the domain
of consciousness. This may be one cause of failure of memory,
and it sometimes causes a failure to remember when there is
no real failure of memory. When one subject dominates the
mind, sufiicient attention is not given to other subjects to
secure their retention. Hypochondriacal patients often pre-
sent this inability ; their minds are constantly occupied with
their own feelings, and they do not give sufiicient attention to
other subjects to ensure ihevr persistence in the mind, and the
apprehension of mental failure is added to the other sources
of mental distress. Reassure the patient as to his fancied
ailments, and the unmeaning character of his various sensa-
tions, and his loss of memory will vanish.

Closely connected with failure of the power of attention is
incoherence of idea. Instead of the definite sequence of
mental processes that we recognize as normal, one mental
image excites another by some accidental association, which
would be unnoticed in health. Often the connections that
determine sequence are so subtle as to evade detection. The
mental processes change rapidly, and when one is only half
expressed, another has possession of the mind. This inooher-

MENTAL FAILURE. 119

ence is conspicuous in delirium, and is also frequent in simple
mental failure.

Defect of moral sense is also common in mental failui'e.
The slighter defects are relative, rather than absolute, and
must be estimated by their deviation from the normal conduct
of the individual. Many actions would be more distinctly
pathological in a man of refinement than in an ill-mannered
man of the lower classes. Other actions are unequivocal.
Urine and stools are often passed into the bed in cases of
brain disease, in consequence of this mental failure, when there
is no loss of power over the sphincters. Under these circimi-
stances it is an indication of a considerable degree of mental
change — a greater degree than is suggested, perhaps, by the
other indications of the mental state. Of similar significance,
in these cases, is a disinclination to swallow. There is no
real difficulty in deglutition, but when food is placed in the
mouth, the patient lets it lie there, and after some time,
perhaps half an hour, spits it out again. Particles may get
into the larynx, and suffgest that there is a pharyngeal
p».l,d. SZ. not A ^. It is bnporlt Zot,
that, in children, slight mental defect is often shown by a lack
of the sense of propriety, rather than by failure of mere intel-
lectual processes. They are unabashed by' the presence of
strangers, are disobedient, mischievous, meddlesome. Indeed,
the lack of capacity for restraint often leads to undue mani-
festation of what mental power they possess, and parents
constantly consider such children unduly precocious, and
possessed of mental faculties above the average.

LECTUEE X.

SYMPTOMS (Contim^d): AFFECTIONS OF SPEECH.

Q-ENTLEMEN, — From the mental symptoms that we con-
sidered in the last lecture, we pass now to another group, inter-
mediate between the mental symptoms on the one hand, and
simple motor and sensory symptoms on the other — ^affections
of speech. We must consider them at some length, because
the phenomena are complex, their relations are intricate, and
if I were to attempt to be brief, I should succeed only in
being unintelligible. As it is, I fear I must ask for your
somewhat close attention. There is difficulty, not only in
the theoretical study of the subject, but also in the practical
application of our knowledge. No two cases of speech-
defect are alike ; and you can only unravel the phenomena
of each case by having a firm grasp of the laws that govern
both normal speech and the derangement that is produced
by disease.

The brain contains upper and lower mechanisms for
expression by articulate speech, the upper in the cortex, the
lower in the medulla. The latter transfers to the peripheral
nei'ves the impulses that come down from the coi-tex, perhaps
adjusting their form in minor details. It is in the cortex
that the elements of speech are arranged. In disease of the

AFFECTIONS OF SPEECH. 121

lower mechanism, the elements of expression are eoireet in
nature, number, and arrangement, but their form is defect-
ive ; "articulation " is at fault — ^the jointing of the elements.
In disease of the higher cerebral apparatus, the form of the
constituent elements may be correct, but they are wrong in
nature, in number, or in arrangement. The error in the
arrangement of the elements often causes great error in the
form of words, although the form of the elements may be
correct. You will understand this better as we proceed.
We have already considered the effect of disease of the
lower mechanism in the medulla, and are now concerned
only with the cortical mechanism.

Speech is the expression of mental processes; but it is
not the only mode of their expression. They may also be
expressed by writing; but writing is merely expression by
speech translated into symbols of a different kind. The nerv-
ous processes are elaborated in the same cortical mechanism,
although they leave the cortex at a different place, and do
not pass through the lower mechanism for articulate speech,
but pass by it, to still lower mechanisms in the spinal cord.

A different and very important mode of the expression of
mental processes is by simple muscular movements in various
parts of the body — ^f ace, limbs, and even trunk ; we call these
"gestures." Gesture-symbols are much simpler than speech-
symbols. They are the first to be acquired by the race and
by the child — the most uniform in different races. Speech-
symbols are acquired later, and are diverse in different races.

By these methods we express two classes of mental pro-
cesses — " ideas " (which are expressed as propositions) and
emotions. Emotional processes are by far the simpler, and
they are expressed by the more simple and automatic
methods, chiefly by gesture. This is the chief use of
gesture. It is true, gesture can express propositions, but
only in a very limited degree, and only those that are
extremely simple in character. An instance is the expression
of affirmation by a nod. Gestures that express propositions
are called "signs."

In vocal speech there are two elements — articulation and

vex I.ECTITllE X.

phonation. Articulation fomis the words on fLe outgoing
current of air ; the larynx adds voice to speech, and enablt's
it to be heard at a distance. Voice is merely material for
articulation. It is indeed a means of expreBsion, hy its
variations, but it is only an expresaional gesture accom-
panying speech, and, like other gesturcB, it expresses chiefly
emotions. Emotions may also be expressed by words, as by
interjections, and by many phrases that have a propositional
fonn, but only an inter jeetional meaning—" dead proposi-
tions," they have been aptly termed by Hugblings-Ja^tson,
to whose philosophical investigation of aphasia every student
of the subject is profoundly indebted* Most oaths are such
"dead propositions," and so are many familiar expressions,
as when, to express mere surprise, we formally deny, as in the
phrase, "Tou don't say so!" Eeal propositions, as such,
cannot express emotion, they can only state the fact of its
existence. Although tone chiefly expresses emotion, it has,
like other gestures, a limited power of convejrng propositions,
as when a negation is converted into a question by an inter-
rogative tone.

The expression of emotion is essentially involuntary and
automatic. The wiU is needed, not to effect it, but to
restrain it. The expression of propositions is chiefly volun-
tary, by an effort of the will. But propositions differ much
in their speciality. The more special, the less frequently
expressed they at'e, — the greater is the volition required,
although we may be scarcely cunscious of it. The less
special, the more frequently employed they ore, — the less
voluntary', the more automatic is the utterance. In vt>c«,l
music, words are chieily used as the vehicles for tone. The
propositions that the words formally convey are scarcely ever
really expressed as such.

• Of Dr. HughliiLgs-JackBon'B writings on the subject, the most important
are his papera in "lirain" (vol. i., p. 305 ; ii., p. 203,323). TheatuJi'ntwlio U
iutcvestfil ill the siihject ia strongly ttilvised tii read these articles, Tliosu
who sre acquaiuted with them will see how largely the views expreatieil in
this lectnre have been monldedby those of Dr. Jacksou, audhowesttensivel; I
hare adopted tlie phraseology that he lias made, not only current, but
ijuliajyjnsalilc.

AFFECTIONS OF SPEECH. 123

Intellectual processes are aroused by language as weU
as expressed by language — aroused through the senses of
hearing and of sight, and in blind persons by touch. This
necessarily involves an intimate connection between the
nervous processes for these sensations and those for language.
Of the links of this connection we can recognize some,
because disease occasionally separates them. When a word
is heard, the processes thus aroused in the auditory centre
excite others that subserve the recognition of the sound as a
word, and these, in their turn, excite those that subserve the
image corresponding to the word. So too with visual word-
symbols. Thus the nervous processes for language have
both motor and sensory relations. Of these, the sensory
(auditory) processes are developed earlier than the motor
processes. The child understands many things said to him,
long before he can utter a single word.

We have seen that a sensory word-process must intervene
between that for the sound and that for the image of
the thing symbolized. So motor word-processes intervene
between those for the image and the motor impulses for the
muscles. There is a sort of internal revival of words before
they are uttered, and this may occur without utterance. A
revival of word-processes, motor or sensory, often accom-
panies deliberate thought.

The motor and sensory word-processes leave behind them
residual states, which facilitate the subsequent revival of the
same arrangements. These residual states subserve the
memory for words. We have seen that memory of other
kinds is subserved by similar residual states (p. 117). Thus
there may be said to be both a motor and a sensory memory
for words. In the revival that precedes speech, we are
more conscious of the motor process, of a sort of " internal
speech." But it is probable that both motor and sensory
word-processes occur together, and that the sensory (auditory)
word-process actually leads in the revival. This process, as
we have seen, is first established. It may be perfect when
the motor memory is lost, and its loss interferes with
thought far more than does the loss of the motor memory.

124 LECTUKE X.

In the act of reading words, the process is analogous l
that which takes place in hearing spoken words. Nerve-
prnoesaeH are aronsed sutcessively for the simple sensation,
the word-symbol, and the image of the thing symbolized.
There is an intimate connection between these sensory pro-
cesses and the motor process. In those unaccustomed to
reading, the motor processes are energized in the act, and
even the lips may be observed to move, mental images being
no doubt aroused more readily by the double than by the
single process. In the act of writing, the motor processes
for articulate speech are first energized, and these excite the
processes for the movement of the hand, and the formation
of the written symbols. Eveu in writing, however, it is
probable that the auditory nerve-processes are revived before
or with the motor processes. If you attend to the mistalies
you make in writing — writing wrong letters, for instance —
you may often traee the influence of these auditflry and
motor associations by the character of the error.

We may now ask what we know as to the parts of the
brain concerned in these functions. The chief facts have
already come under our notice in our review of the anatomy
of the brain. In each hemisphere the lower part of the
ascending frontal convolution contains the centres for the
movements of the muscles concerned in articulation. From
these centres, conducting fibres pass down to the lower
mechanism. Hence motor processes for words must leave
the cortex at this part. The adjacent posterior pajt of the
third frontal convolution also contains structures that sub-
serve speech, perhaps somewhat higher processes than those
of the motor centres in the ascending frontal, and this region
is usually regarded as the chief speech-centre. Wbefher the
island of Eeil contains similar structures is still uncertain.
The first tempore -sphenoidal convolution contains the stme-
tures that subserve the auditory perception of words. Those
for the visual pereeptiou of words are probably contained in
or near the angular gjTUS. But there is an important
differeuce in the functions of the two hemispheres. Volun-
taiy speech-processes go on chiefly in the left hemisphere in

AFFECTIONS OF SPEECH. 125

right-handed persons, in the right hemisphere in left-handed
persona. The senBoiy word-processes, perhaps influenced by
the motor, also go on chiefly in the left hemisphere. Disease
of the left motor speech-region causes loss of the power of
uttering words voluntarily; and that of the first temporal
convolution, loss of the power of understanding spoken
words — "word-deafness;" whereas disease of the corre-
sponding regions of the right hemisphere produces no such
efEect, The power of understanding words that are seen is
also localized in the left hemisphere. Thus, althotigh the
sensory centres for hearing and sight are double, one in each
hemisphere, it is only in the left that they subserve the
recognition of words.

And yet the left hemisphere has by no means a monopoly
of speech-function. The right hemisphere contains structures
of similar position and similar connections. These structures
can supplement those in the left hemisphere. Loss of speech,
due to permanent destruction of the speech-region in the
left hemisphere, has been recovered from ; and that this
recovery was due to the supplemental action of the corre-
sponding region of the right hemisphere, is proved by the
fact that, in some of these cases, speech has been again lost
when a fresh lesion occurred in this part of the right hemi-
sphere. This supplemental action occurs in the sensory as
well as the motor functions. It oeciu« far more readily in
children than in adults. Permanent aphasia in children
from disease of the left hemisphere is almost unlmown. The
loss of speech rarely lasts longer than a week. Then the
child speaks almost as well as ever. Hence it is probable
that speech-proeeeses go on more equally in the two hemi-
spheres in childhood than they do in adult life. It is also
highly probable that there are individual differences in this
respect among adults. Certainly, with a lasting lesion, speech
is recovered more readily by some than hy others. But in
all persons the right hemisphere takes some share in speech-
processes. Much emotional expression and automatic use of
words is effected by it. This is shown by the fact that such
emotional and automatic use of words remains, although

126 l.FXTL'liE X.

the voluntary iise of words is lost by disease of the left
hemisphere. But since emotional and automatic espression
is not lost from disease of the right hemisphere, it foUows,
as Hughlings-Jaokson has insisted, that such expression
must be effected by both hemispheres. Hence we may say
that expression is one-sided, that is left-sided, in proportion
as it is voluntary ; is both-sided, that is either-sided, in pro-
portiou as it is involuntary and automatic' We have seen
that the same law holds good of motion generally. Dr.
Jackson believes that the preliminary energizing of motor
word-processes that precedes utterance takes place in the right
hemisphere. Perhaps, however, it occurs in both.

A curious illustration of the analogous motor impairment
was presented by a man who had right hemiplegia and
aphasia. In these cases there is usually more loss of simple
voluntary movement of the tongue than in similar disease
of the right hemisphere, aa if the speech pre-eminence of the
left hemisphere carried with it a greater representation of
the simpler movements of the tongue. I told the man to
put out his tougue. He made many attempts, but could
not. Then he put out his tongue and licked his lips—
an automatic action to facilitate the process, — and tried
again to put it out voluntarily, but failed. An analogous
speech-defect was that of a girl who, after many vain
attempts to utter the word " no," said, " I can't say ' no,'
sir."

The extent to which automatic word-processes may be
subserved by the right hemisphere is strikingly exemplified
by a case that was under my observation many years ago.
A man had eraholiam of the left middle cerebral artery, and,
as we afterwards found, the whole of the motor speech-region
of the left hemisphere was destroyed. From the attack till
his death, a few weeks afterwords, he said only " yea," " no,"
and once uttered "uing," when the house physician wished
hi in good-moming. But one day another patient in the
ward began to sing a song,— "I dreamt that I dwelt in
marble halls." The speechless patient joiood in, sang the
fii-at vei'se with the other patient, and then sang the second

AFFECTIOXS OF SPEECH. 127

verse by himself, uttering correctly every word. Of course this
was not speech. No one intends to express the propositions
contained in the words of the song. The words are used
automatically, and this automatic utterance must have been
effected by the right hemisphere.

In all cerebral affections of speech there are two elements
to be distinguished : some speech is lost, and some speech is
preserved, but is deranged. The loss is the effect of the
destruction by the lesion ; the derangement of the remaining
speech is due to the imperfect action of the speech-struc-
tures that remain. The word " aphasia " is current as a
general designation for all forms and degrees of loss of
speech, as "ansemia" is for all forms of defect of blood.
Other general terms have been proposed, equally inexact,
and less convenient. Indeed, the whole subject has afforded
abundant scope for word-makers, who have flooded its litera-
ture with a new terminology, to a large extent needless, and
to some extent injurious, fostering a harmful tendency to
divide where it is desirable only to distinguish. One recent
writer alone proposes fifty special designations for varieties
of aphasia.

The two most important symptoms of speech-defect corre-
spond to the motor and sensory functions already described.
(1) In some cases there is loss of the motor processes for
speech. The patient can understand what is said to him, but
he cannot speak, or can only use voluntarily one or two
words ; he cannot even repeat words. (2) In other cases the
patient is unable, sometimes absolutely, to understand what
is said to him. In this case, he has usually considerable
power of speech, but makes mistakes in words and in their
form, especially in unfamiliar expressions. The error may be
so great that his speech is unintelligible. In the first case the
patient is conscious of his errors ; in the second he is not,
because he does not imderstand his own utterance. These
two leading varieties of aphasia are best styled (with
Wernicke) motor and sensory aphasia.

But another defect is very common. There is an inability

138 I.EtTUBE X.

to revive voluntarily the word-images, or flieae are revived
wrongly. The patient cannot " recollect " the word, or he
reooUscts it wrongly. Defect of memory being termed
"amnesia," this special fonu is termed "verbal amnesia,"
or sometimes " amnesic aphasia." "We have seen that in the
revival of words both the motor and the sensory memories
take part, but the sensory (auditory) is the more important,
and takes the lead. Doubtless, in educated persons, the
visual memory assists ; but we may, for the present, leave
this out of consideration. Word- deafness involves loss of the
auditory word-processes — loss, that is, of the leading mechanism
for the subjective revival of words. It always, therefore,
involves verbal amnesia. In motor aphasia there is much
less verbal amnesia, because the sensory processes are intact ;
the loss of the motor memory probably causes some impairment
of the power of recalling words, some verbal amnesia, although
the loss is difficult to ascertain on account of the loss of
speech. But verbal amnesia may exist mthout word-deafness,
without any impairment of the power of expressing words.
The patient cannot " think of a word " ; hut if it is told him,
he utt«rs it correctly at once. As a ciiiucal variety of speech-
defect, this form is often met with, but it is not a sepai'ate
pathological form, as it has sometimes been regarded. It has
been described as the loss of a special memory for words ; but
there is no function or seat of memory for words, except that
of the word-processes, motor and sensory. Moreover, the
defect in word-revival always occurs in a certain order, from
the special to the general. Its indication is that the speech-
processes go on in structures that are relatively inadequate.
The loss is never absolute ; and it is always a defect in the
voltintav'j revival. Automatic utterance is largely in excess of
the voluntary utterance. Conclusive evidence that it is not a
distinct pathological variety is afforded by the fact that the
moat perfect example of this amnesic aphasia is presented
hy cases in which there has been, at first, complete motor
aphasia, and, the lesion persisting, the patient has slowly
recovered a considerable power of speech, by a re-education
of the right hemisphere. Here it is manifestly a residual

AFFECTIONS OF SPEECH. 129

state, the result of the relative inadequacy of the structures
in which the speech-processes go on.

We may now consider the varieties of aphasia, and the
various symptoms in detail, premising that they are often
combined, and the resulting symptoms are often extremely
complex.

In extensive disease of the motor speech-region, the de-
rangement ULSually extends beyond the limits of vocal speech.
The power of writing is lost, even when there is no paralysis
of the hand. This shows, as I have already said, that in writ-
ing, the word-processes, although they must leave the cortex
at the hand-centre, are iSrst energized in the speech-centre.
In severe cases, expression by gesture is at first impaired, so
far as the expression of propositions is concerned. The patient
nods for " no " as well as for " yes." But all power of expres-
sion is never lost. That whichremains varies much in different
cases, but is always the more automatic — ^the least special
forms of expression. Emotion may be expressed by gesture
perfectly, and even by words, interjections, or phrases,
such as oaths, that have a prepositional form but not a
propositional meaning. The oath uttered in anger cannot
be repeated without the emotion. Further, most patients
speedily regain one or two of the lowest propositional utter-
ances, as " yes " and " no." The word " yes " seems to be
a less automatic utterance than the word " no." Children,
as a rule, say " no " long before they say " yes." Perhaps
these words are first regained because they are often used as
interjections ; they may be first regained as interjections,
and this may facilitate their propositional re-acquirement.*
These patients may also sing, as did the man whose case I

« ((

The words * yea * and * no * are propositions, but only when used for
assent and dissent ; they are used by healthy people interjectionally as well
as propositionally " (Hughlings-Jackson). A child under my observation,
in learning to speak, first uttered **no," and then expressed assent by the
common infantile afl&rmative **m'm." This he next elaborated into **am,"
and for many months after he had become able to speak well, he still used ' ' am "
to express assent. When he began to say "yes, " he employed it for a long time
only as an interjection, e.g.^ when he was called, retaining "am" for assent.

K

130

have mentioned. In extensive and peraistent disease of
left hemisphere, all the utterances must be effected through
the right hemisphere. In rare cases, under strong emotion, a
proposition may escape that is much higher than the habitual
Titteranoe of the patient, forced out, as it were, by the emo-
tion (Hughlings-Jaokaon). Slowly, more power of speech
returns, by the re-education of the right hemisphere ; and,
as I have said, more readily in some persona than in others,
and most readily in children

Motor loss, such as this, usually resiiltfe from disease of the

i

FlQ. 18.— DiAR&AM or PKOBABLB Cl>fR9E OF FiBEBS FROM MOTOB Sl'EEfH-

Centhe.
A, hand-centre in the middle of tlie ascending frontal conrolutioD ; A m,
flbrBB from this to internal iMipsule ; 8, motor speech-centre ; S C, fibres
from this to the corpus callosum ; and S in to the internal capsule.
S A, fibres from speeoh-oontiB to haud-centre. A lesion at m i« will
came only transient aphasia, the speech -processes being able to poas
hy 8 C to the eorpns eallosum and opposite speech-region ; a small
lesion at x would caiase permanent aphasia, since it involves both the
fibres to the corpus callosom and internal capsule, bnt would not abolish
expression hy writing, the fibres S A (connecting the speech- and hand-
centres) escaping.

cortex; hut it may also be caused by disease just below the
cortex. If the disease involves the motor path some distance
below the cortex, it may cause transient defect of speech ; but
this is soon recovered from, probably because the left region
is able to act through the right by means of the conmiiBBural

AFFECl'IONS OF SPEECH. 131

fibres of the corpus callosmn. When the disease is just
beneath the cortex these fibres are also damaged, and the
aphasia is as lasting as when the cortex itself is destroyed.
In the extremely rare cases in which a patient can write and
cannot speak, the disease is probably so placed as to interrupt
the fibres that go to the motor tract, and those to the corpus
callosum, but has not destroyed the speech-centre itself, or
the connection between it and the hand-centre (see Fig. 18).
The next important point to be considered is the error that
occurs in the speech that still remains, or has been regained.
This speech is frequently wrong, both as regards the words
employed and their form. The error in form is not in
articulation, but in the elements of the word. One patient,
for instance, said "int" for "ink," "tinors" for "scissors" ;
another asked for some "pagne-cham" when she wanted
some champagne. The error in form may be so great that
the speech is unintelligible jargon; one patient could only
say " drumlandee." The resulting disorder is often termed
"ataxy of speech." Hence, this form of speech-defect is
often termed "ataxic" or "atactic aphasia," an objectionable
designation for the pathological variety, because equal
" ataxy" may result from the opposite defect, a sensory loss,
word-deafness. Moreover, the term is apt to mislead, sug-
gesting that there is a centre or faculty for the co-ordination
of speech other than the motor speech-centre.

Without error in form there maybe error in use: if "yes"
and " no" are the only words that can be uttered they may
be used wrongly. When more speech is retained, an unin-
tended word may be used. Errors occur, just as loss occurs,
in proportion as speech is special and voluntary. There is
always less error in automatic utterance and in signs.
A patient who can only say "no," and utters the word on
all occasions, may indicate correctly by signs, by nodding or
shaking his head, whether he means "yes" or "no." It
is often difficult, sometimes impossible, to understand the
mechanism of these wrong utterances, but they may be, to
some extent, understood by certain general principles. The
first is the tendency to repetition. This depends on the fact,

K 2

132 I.ECTl'RE X,

that a nervous arrangement, after functional activity, remains
for a time in a condition in wMch it is more readily energized
than other nervous arrangements. This often leads to error
in health. If Smith has been talking to Jones of Robinson,
he is very likely to call Jones "Mr. Robinson." It ia by
this tendency to repetition that recurring utterances of what
Dr. Jackson calla " low speech value " become established.
In the speech-structtires that remain, if one arrangement
has been energized, it is apt to bo re-excited on every
attempt, to speak, and the more often the words have been
uttered, the greater is their tendency to come out. It is
easily oonoeivable that the right hemisphere may suffice
for recurring utterances of low propositional value, such as
"no, no.'" But in some patients the recurring utterance is
of high propositionftl form, although used without meaning.
The character of this utterance is often so special as to sug-
gest, irresistibly, that it has its origin in some former utter-
ance of the patient. Dr. Hughlings- Jackson has suggested
that it is the expression that the patient was about to utter
when taken ill, and that such recurring utterances occur only
in the cases in which the onset was deliberate, believing that
it is the result of a preliminary speech-process in the right
hemisphere. I am inclined to think that it is usually the hist
words actually uttered by the patient, just before the attack.
These cases support the view that in ordinary speech the right
hemisphere takes a part in the prebminary energizing of the
speech-processes, siuee such a recumng utterance can only
he efEected through the right hemisphere. In the absolute
aixest of voluntary speech-processes that follows an extensive
lesion, causing aphasia, the process last energized in the right
hemisphere, if energized not long before the attack, is re-
energized when any attempt to speak is made and is uttered,
no fresh arrangement being possible to the will for a long time.
Many facts support this explanation of these reciuring utter-
ances. Thus, the recurring utterance of a signalman who
was seized when on duty, was " Come on to me" ; that of a
girl attacked when riding on a donkey, " Gee, gee" (Hugh-
lings-Jaekson) ; that of a librarian was "List complete"

AFFECTIONS OF SPEECH. 133

(Eussell). One of my patients was taken ill in a cab; on
entering the cab she had told the cabman to drive her to
"Mrs. Waters," and these were the last words she spoke.
Her recurring utterance was "Missis." The recurring utter-
ance may be an unmeaning combination of syllables. Dr.
Jtickson has suggested that the disorder is due to the struggle
of various word-processes thai arise simultaneously, and of
which only fragments succeed in achieving expressional pre-
dominance. Some of the error in form may also depend on
the fact that relics of previous word-processes get mixed up
with those that the patient intends to utter, in consequence of
the readiness with which the former are re-excited. This is
often obvious on an attempt to repeat the alphabet, which one
patient uttered thus : a — a, h — ^be, c — ce, c? — de, e — de, / —
def , g — de, h — a, j — da, k — ^ka, I — ^kel, m — em, n — den, o — do,
p — ^be, and so on. In the same way, the elements of the
recurring utterances are apt to crop up when the patient
begins to say other words, and so also, perhaps, are parts of
words that have been familiar in previous life. Another
curious and common form of error is the reversal of the sylla-
bles of a word, as in the instance of " pagne-cham," already
mentioned. As I have said, words are revived subjectively
before they are uttered, and it would seem that the part of
the word last energized is the most vivid and most readily
uttered. I have heard a very young child say " I got for,"
instead of " I forgot." The reversal is sometimes partial; an
obtrusive consonant in the middle of the word may be uttered
also at its commencement: one patient said "Lalice" for
"Alice." Often the recurring utterance is a repetition of the
same consonant with varying vowel sounds. One patient,
whenever he tried to speak, always uttered, "da, de, da, do,
de, da," with extreme rapidity, like an engine- wheel flying
round on a slippery rail. This is evidently explicable on the
principle of repetition. What consonant is the basis of this
utterance is doubtless determined by circumstances similar
to those that determine the form of the recurring utterance.
The woman whose chief utterance was " Missis," when she
acquired some additional power of speech, and tried to

134 LECri'RE X.

utter other words, was apt to run off into "so
se, 80, si."

The losB of writing may he absolute ; the patient can only
make unmeaning strokes ; or letters may be formed, but
<'-ombined at random. Lastly, words may be written, but
erroneously. The errors may be similaa- to those that occur
in speech; repetition of words and syllables, and the substitu-
tion of one letter for another, often of one that is aunilar in
sound, as^) for l>, sometimes one that is written in a similar
manner, as g for a. Sometimes the order of the letters of a
word are reversed ; one patient wrote " tae " for " tea." The
meehanism of these errors is doubtless the same as that of
the similar errors that occur in speech. The same law of
order of loss is traceable. It is common for a patient t« be able
to sign his own name when he can write nothing else, just as he
can tell you his own name when he can say nothing else. A
man's own signature is the most automatic of all his writing.
One patient, being told to \vrite his own name, wrote "James
Slim," correctly. He was then told to write how he came to
the hospital, and he wrote " cgng kgig feiyan." The errors in
writing are usually greater than in speech, as indeed they
are in health. In the double symbolism there is more room
for error, and there is more time for error. Thus, when the
patient who wrote as above was asked to sni/ how he came to
the hospital, he said "rail"; asked "how else?" he said
"elab"; asked again, " no way."

Patients who cannot write a word can often copy writing
or copy print in printing characters, sometimes in writing
characters ; but they do not understand it, and copy mistakes
without correcting them. I remember a sad instance of this.
The son of a distinguished poetess would copy page after
page of his mother's poems, although he clearly could not
understand them. He would also copy, with perfect exact-
ness, page after page of a complicated almanack — always in
printing characters.

In the defect in the subjective revival of word-processes
that is termed verbal amnesia, the order of loss is also from
the special to the general. Proper names are lost first, and

AFFECTIONS OF SPEECH. 135

nouns are lost before verbs and adjectives. This loss for
nouns has been described as a special variety of aphasia, but
it is only a special example of a general and almost universal
law. Among nouns, cwteris paribm, the more special are lost
first, the more general being retained and more easily
recalled. Thus, one patient, being shown a shilling, and
asked what it was, replied "money," then, after a pause,
"coin," and at last, after another pause, " shilling." There
is often error in utterance in this form of speech-defect. The
patient uses a wrong word; asks for a spoon when he wants
a fork. Sometimes, with a little care, we can trace the
mechanism of these wrong words. Thus, one patient with
some word-deafness, but no motor loss, on being shown a
pen-knife and asked what it was, said " Cornwall." Further
investigation made it clear that the patient had only used a
similar knife for the purpose of cutting his corns : hence the
sight of the knife led to the energizing of the nerve-processes
for the word " com." He had once lived in Cornwall, and
so the processes for the word " com " led to the energizing of
" wall" in association with "com," rather than of " knife."
In considerable degree, especially when there is loss of
the auditory word-processes (word-deafness), there is con-
siderable error in the forms of words, because the patient is
thrown upon his motor memory, and this is apt to mis-
lead him when it has not the co-operation of the sensory
memory. No doubt this mechanism was at work in the
energizing of " Cornwall," just mentioned. These patients
have often an extensive power of expression by familiar
phrases, if they bring them out quickly and almost auto-
matically; if they hesitate they get wrong. "If I want to
say a thing I must say it in a hurry, or I cannot say it at
all," one patient said. Errors in writing are more marked
in these cases than are the errors in speech, for the reason I
have already mentioned, and we can often trace their origin.
A patient who made no mistakes in speech wrote "disacree-
able" for disagreeable, "glag" for glad. The former was
evidently due to an error in the motor memory, substituting
for one letter another for which the motor process is nearly

130 LECTURE X.

the same ; the second was due to the principle of repetition.
The neiToua arrangements are not under perfect control, and
some unintended aixangenient is energized, in which, for
one of the reasons ah^ady mentioned, the r^stance is
lower. I may quote an instance of the greater readinesa of
familiar automatic utterance than that which is less familiar,
and therefore requires a greater voluntary effort. I asked
the patient who had made the remark just quoted about
saying things in a hurry, to write down the name of a boat-
race that had taken place the day before. He said, " Boat-
race ? Oxford and — Oxford and Gate — Ama — Abramidge —
Oxford and Baxford — I ought to know, I have been there
often — what is it ? — Oxford and — now I cannot tell you —
Oxford and Batham." He then took the pen and wrote
" Oxford," and said, " Now I cannot say that other," and
wrote "hah a tha," and then "Oath h," and exclaimed
"I am a bigger fool than ever. Oxford and Ca — Cab — Caba
— Cambridge — ^there, I have it at last." But after repeating
it correctly several times, he wrote " Cabrage."

In partial word- deafness, the same order of loss is observed.
The patient may understand familiar words, and not those
that are unfamiliar. He may understand signs when he does
not understand speech. If told to put out his tongue, he
may make no attempt to do so ; but if shown, he may put it
out at once. Putting out the tongue is not, however, a good
test. When a patient comes to a doctor, he expects to be
told to put out bis tongue, and may guess that this has been
said to him. He may put out his tongue to order, but if told
afterwards to shut his eyes, he may simply again put out his
tongue. It is, perhaps, hardly accurate to speak of this as
guessing. Expectation faeihtates comprehension. This state-
ment is a platitude : but the physiological aspect of the
platitude is that the physical side of " expectation " is a
lowering of resistance in certain nerve-prooesses. Hence it
is better to ask the patient to do something unexpected, or, as
Dr. Hughlings-Jaekson suggests, to ask biTn some absurd
question, the comprehension of which is readily shovra by
the obvious amusement it excites. The same condition ib

AFFECTIONS OF SPEECH. 137

observed in those who are recovering from word-deafness.
Slow recovery occurs from word-deafness, as from other
forms of aphasia, the lesion persisting. Doubtless this also
is by the re-education of the right hemisphere, perhaps
aided by the visual word-centre. A very intelligent man,
who had slowly recovered from complete word-deafness, told
me that he still often had a difficulty in imderstanding a
word spoken to him ; but he would repeat it a few times, and
at last he seemed to see the letters of the word, and then its
meaning flashed upon him.

Patients with motor aphasia usually cannot read. We can-
not infer from this that there is word-blindness, in the strict
sense of the word. The co-operation of the motor speech-
centre seems necessary for imderstanding the visual word-
symbols. The best way of testing the power of reading is
to write down a direction to perform some simple action.
Patients often try to read, and even seem to think that they
imderstand, when they certainly do not. This loss usually
lessens in time, other word-processes that remain aiding the
visual centre. But in true word-blindness the patient is
absolutely unable to understand the words that he sees, and
the loss is the more striking in that the motor processes for
speech are often preserved.

I may briefly recapitulate the chief points to be attended
to in examining a case of aphasia, and the indications
they afford. Remember that some weeks must elapse,
from the time of the onset, before we can infer, from the
character of the symptoms, the position of the lesion.
The connection between the different centres concerned in
speech is such that an acute lesion in one of them causes a
temporary derangement of the others. Only when this has
passed away, in the course of two or three weeks, can we
infer the position of the lesion. The action of the speech-
centres may also be interfered with, for a time, by disease
that is near them but does not actually involve them or the
fibres from them.

It is well to begin by ascertaining whether the patient can

138 LECTURE X.

understand what is said to hira— whether there is any wor^^
deafness. Try him first with simple orders, and then with
sentences that are more complex. If he cannot understand
even simple things, there must be disease of the first temporal
convolution, or heneath it. If there is mere impairment,
and not loss of auditory perception, it may be the result of
partial damage to the same parts, or may be the result of old
disease, from which the patient is recovering by the action of
the right hemisphere.

Next observe the character of the motor loss, the degree of
speech that remains, and whether the patient can repeat what
is said to him. If speech is limited to a few automatic
utterances, and the patient, while understanding, cannot
repeat words, there is disease of the motor speech-region —
third frontal and lowest part of the ascending frontal convo-
lutions. The disease may not be in, it may be just beneath,
the cortex. If utterance is only unintelligible jargon, or if
there is a recurring utterance, the indication is the same. If,
however, there is word- deafness, great formal error in speech
does not prove disease of the motor speech-region. If the
motor loss soon passes away — in the course, for instance, of
two or three weeks — although hemiplegia persists, the disease
is probably some distance below the eortes, in or near the
internal capsule. If recovery takes place in the course of two
or thi-ee months, hemiplegia persisting, the lesion is probably
in the white substance near the cortex, and has damaged, but
not destroyed, the fibres to the corpus caUosum and opposite
speech-region. This is the more probable if the patient can
write better than he can speak. It is often difficult to ascer-
tain the patient's power of writing, because the right hand is
frequently paralysed, and the left hand is awkward, while to
form words with moveable lettera is a much more severe test
than writing.

Inabihty to read can only be regarded as evidence of
disease of the visual word-centre when there is no motpr
aphasia. The power of voluntarily recalhng words is best
tested by asking the patient to name objects that are shown
to him. Defect of this may be due to past or present word-

AFFECTIONS OF SPEECH. . 139

deafness, or it may be a residual condition left by a past
motor aphasia. In neither of these conditions has the
symptom any diagnostic value. It only indicates the relative
inadequacy for volimtary action of the structures in which the
speech-processes go on — ^in most instances those of the right
hemisphere acting with those of the left that remain. If the
condition is a primary one, its significance is uncertain. It is
probably due to a small lesion near the sensory speech-regions
of the left hemisphere, lowering their function generally,
sometimes to one in the parietal lobe. There is no evidence to
support the statement that is often made, that the symptom is
due to, and indicates, an interruption of the connection between
the sensory and motor speech-centres. Indeed, it is not easy
to conceive how such an interruption could produce the effect
ascribed to it.

Motor aphasia is often combined with hemiplegia from
disease of the motor centres adjacent to the motor speech-
region, and especially with paralysis of the face, the centre
for which is the nearest. On the other hand, in sensory
aphasia, hemiplegia is often absent, and, if it occurs, is
usually slight.

In conclusion, one aspect of the question of speech-defect
is of considerable practical importance — its relation to the
capacity for making a will. In pure motor aphasia, in which
the auditory word-processes are intact, words that are heard
are perfectly understood, and assent or dissent can be ex-
pressed, although only by gesture, the patient could certainly
make a will. If there is considerable word-deafness, it is
always so doubtful whether the meaning of what is said
to him is correctly perceived, that there is probably no
" testamentary capacity " unless written words are perfectly
understood, and all communications are thus made. A
fortiori^ if there is both word-deafness and word-blindness,
a valid will could not be made.

LEOTUEE XL

SYMPTOMS {Cmtinued) : HEADACHE— VERTIGO— VOMITING.

Gentlemen, — We will consider next three symptoms that
stand very much on the same level of diagnostic sig-
nificance, — ^symptoms that are often combined, although
they are very different in form and in nature — ^headache,
giddiness, vomiting. The first of these is, of aU the many
symptoms that organic disease may produce, the most
obtrusive, the most distressing; and at the same time the
most equivocal, the most apt to mislead both the patient
and the physician. Local pain is a symptom of universal
incidence; wherever it occurs, it absorbs the attention of
the sufferer, and to him at least, suggests irresistibly a local
cause. But of all seats of pain, the head is the most
common, and pain is here the most suggestive of local
disease, and yet it is the place in which pain is most
frequent without local disease. In consequence of some
mysterious relation, pain in the head is the common result
of most varied causes — of stomach disturbance, of anaemia
and plethora, of every kind of morbid change in the blood,
febrile conditions, acute specific diseases, kidney disease,
toxaemia. The nerves that supply the walls of the skull are
prone to neuralgic pain of every kind. Headache occurs
also in various functional disorders of the nervous system.

HEADACHE. 141

Sly restilta from mechanical congeetion of the brain,
however produced, and is sometimes bo ohtmsive that the
patient notices the cause leas than the effect. Thus I have
known a patient to come for treatment on account of head-
ache, and to complain of nothing else, when the headache
was the result of cough, and the cough of phthisis. I think
it is no exaggeration to say that for one case of headache
due to organic disease of the brain, you will meet with fifty
that are due to other causes.

There is not much in the character of the pain to indicate,
or even to suggest, its origin. Pain that follows closely the
course of a cranial nerve is probably neuralgic in nature ; but
it may be due to irritation of the fibres of the nerve : bo that,
while it does not suggest, it does not exclude, intracranial dis-
eoBe. Pain that is very hmited in area is more often of func-
tional than of organic origin. Thus, pain limited to one supra-
orbital region, or to a spot at one temple, on which the patient
can put his finger, or to a spot at the vertex, is commonly
of functional origin ; the last ia common in hysteria, and is
termed, from the frequency with which it is likened to a nail
being driven in, the " clavus hystericus."

Of much greater significance, though atill not patho-
gnomonic, are the course and severity of the pain, taken
together. A common feature of the pain of organic diaease
is its conatancy. The pain varies in severity from time to
time, but there are rarely periods of perfect freedom. It is
usually a severe pain ; often at times most intense, causing
the patient to shriek from the suffering. In mere severity,
however, the pain of organic disease is rivalled by some
functional headaehea, aa by that of migraine ; but these are
paroxysmal — attacks of intense pain are separated by days or
weeks of freedom, comparative or perfect. The pain of organic
disease persists during the night, and often prevents sleep,
or rouses the sufferer. Functional headaches rarely prevent
sleep, which, indeed, often ends the pain. Whenever, there-
fore, a patient complains of severe pain in the head, ask him
if it keeps him awake at night ; and if it does, you should
think of oi^anio diaease as possible, and search most eare-

fully for any other symptonis. But severity and constauoy
of pain, even together, only mtjgeiit an organic cause ; they
do not prove such cause. Proof of this — or even the high
degree of prohability that, in practical medicine, we have
often to be content with — is only supplied by the association
of headache with other symptoms, diffuse or focal. Of the
diffuse symptoms, optio ueuritis and vomiting are the most
significant. An ophthahnoBcopio examination should never
be neglected in any case of severe headache. If you can
exclude three conatitutional states — considerable aniemia,
kidney disease, and lead-poiaoning, — the coincidence of con-
siderable neiuitis and headache may be regarded as proof
of organic intraoranial disease. To this, and to the signifi-
cance of vomiting, we shall presently retiim.

Always remember, gentlemen, that you can never assume
the converse of diagnostic rules. The presence of a symptom
may be strong positive evidence, while its absence has very
little significancG, and perhaps none at all. This is true
in every department of diagnosis. There is hardly a disease,
usually attended by some prominent and characteristic symp-
tom, that does not occasionally occur without that symptom.
Acute peritonitis, of which intense agony is a character-
istic, may run its course without auy pain. Neither the
absence of pain in the head, nor its trifling character, en-
ables you to exclude either intracranial disease in general,
or any special form of such disease in particular. Cancer is
usually a most painful malady, wherever it occurs ; all
tumours of the brain usually cause intense suffering: and
yet cancer of the brain is occasionally almost painless.
I do not say that the absence of symptoms has no nega-
tive value ; it justifies you in attaching leas weight to
equivocal symptoms that are present, but it does not lessen
the significance of any unequivocal symptoms.

We know little of the way in which pain in the head is
produced. The brain of an animal can be cut or torn
without the creature showing signs of suffering. But the
aigmficauce of this fact may be over-rated, since other struc-
tures, that seem normally insensitive, become acutely painful

HEADACHE. 143

when diseased. It is certain, however, that the membranes
are very sensitive, and highly probable that much of the
pain of intracranial disease is produced in them. Some
diseases, as tumour, have been thought to cause pain by
the pressure they produce, but the evidence that this is
commonly -the effective mechanism is insufficient, since
other diseases may increase the intracranial pressure, locally
and generally, without causing pain. Nor can we reason-
ably invoke the ready explanation of " congestion " as a
universal mechanism ; in many conditions of headache this
is out of the question. In sho?^, imtil we know more
than we do at present, speculations as to the way in which
headache is produced are scarcely profitable.

The question may perhaps have occurred to you — ^Is there
any relation between the seat of pain and the position of
the lesion ? All that can be said is, that there is some-
times no correspondence, sometimes there is a general corre-
spondence, and occasionally there is a close correspondence.
Pain at one part of the skull is rarely caused by disease
at an opposite part of the brain ; one-sided pain is
usually due to disease on that side ; disease beneath the
tentoriimi generally causes pain at the occiput, which may
pass down the neck ; and disease at the surface of the brain
often causes pain corresponding closely to the seat of the
lesion. Light percussion sometimes elicits tenderness over
the seat of the disease — ^pain being produced by a tap
there, and not elsewhere. This is most frequently the case
when the disease is superficial. The relation of pain to the
nature of the lesion we shall consider in a subsequent lecture.

Unpleasant cephalic sensations, other than actual pain, are
very rarely caused by organic disease. When they occur
without pain, they are almost always of functional origin,
and suggest the absence of organic disease. The sensations
are, however, frequent elements in the diagnostic problem,
because they distress the patient, are apt to be brought on
by brain-work, and, if allowed to do so, may practically
incapacitate their subject. They generally occur in hypo-

144 LECTURE XI.

ohondriacal persona, who attend much to their sensations, and
to whom these feelings are fertile in suggestions of evil. In-
deed, hypochondriasis often results from, when it does not cause,
these sensations, and it is always inereased by them. They
are common in those whose brains are overworked — in clerks,
in lawyers, in commercial men, — and are predisposed to by
neurotic inheritance, and by the condition of defective tone
of the nervous system that it is fashionable now to dignify
irith the name of " neurasthenia," at onee more alarming,
and more gratifying, to the weakened mind, than the older
equivalent, "nervous weakness," These sensations are
various in character, but feelings of fulness in the head,
heat, "rushing" sensations, and pressure on the vertex are the
most common. The vertical pressure is especially frequent
and troublesome. These feelings apparently depend on an
abnormal consciousness of processes that should not rise into
the sphere of consoiotisness. An infinite nimiber of im-
pressions must be continually reaching the brain from various
parts of the body, engendered by processes of function and
nutrition. Of most of these we are uormaUy unaware, but of
some we may become conscious by attention. Fix your at-
tention on any part of the body, and in a few moments you
will be conscious of some feehng there of which you were
previously imaware. Let it he the vertex : in a few moments
many of you wiU he conscious of a distinct sense of pressure
there, most readily if you are tired — if you have been listening,
for instance, to two or three lectures — or if you are somewhat
out of health. Tou can understand how such a sensation, by
continued attention — aided by that potent intensifier, concern
— may be cultivated ; the sphere of consciousness, as it were,
being extended in that direction, until the sensation becomes
a real trouble, and the sufferer is convinced that there
must be an organic cause for that which is so distressmg.
This conviction, I regret to say, is sometimes strengthened
by members of our profession who find it profitable to pander
to these morbid tendencies by a diagnosis of some actual
disease in harmony with the patient's fancy — a diagnosis for
which there is not the elightest justification. " Congestion

HEADACHE — VERTIGO* 145

of the base of the brain " is one of the most common of these
diagnoses. There is a current manual of diseases of the
nervous system, in which the symptomatology of congestion
of the brain has been largely written from the history of
these sufferers from cephalic sensations. Endeavour to con-
vince the patient that there is no actual mischief in brain or
circulation ; encourage him to disregard the sensations, and
they will slowly cease to trouble him.

There is only one condition in which these sensations, other
than pain, are suggestive of real disease, and that is when they
are distinctly paroxysmal and the paroxysms are accompanied
by vomiting. Not long ago I saw a man who complained
of occasional sensations of a "rushing " feeling passing from
the occiput to the vertex. These gradually increased in
intensity, until the sensation became actually painful, and
with this he would sometimes vomit. There were no symp-
toms of organic disease, with one important exception — ^there
was slight optic neuritis. This gave additional significance
to the vomiting, and made some form of tumour highly
probable. A few weeks afterwards he complaiQed suddenly
of acute pain in the head : while describing it to his doctor,,
he lost speech; he became imconscious, and died in a few
hours. Most likely he had an intracranial aneurism, the
rupture of which caused his death.

We pass next to a symptom that has excited much interest,,
on account of its peculiar character, its significant associations,
and its relation to the disturbances that can be produced
experimentally ia animals. "Vertigo," I need not remind
you, means " a turning." The word is strictly applied only
to those sensations in which the patient feels as if ha
were turning round, or at least moving, or has the related
objective sensation that other thiags are moving before him
in a definite direction. But it is often, and its English
equivalent " giddiness " is still more frequently, applied
to all sorts of sensations that involve a sense of imcer-
tain equilibrium, and even to vague feelings of mental

L

p

146 LECTUKE XI.

confusion, or to dimness of sight — sensations that i
termed " dizziness." Some mental confusion is no doubt
always involved in the derangement of the perception of the
exact relation of an individual to his environment that con-
stituteatnie "vertigo." It is not surprising, therefore, that the
same term should be applied more widely to a similar mental
state, irrespective of the precise mechanism by which it is
produced, especially since our vocabulary is inadequate to
designate, or our language to describe, a hundredth part of
the vaned sensations to which our frame is subject.

We are now concerned only with the Bensations that do
involve so distinct a sense of disturbed equilibrium or actual
movement as to come under the general designation. In
definite vertigo we may distinguish three elements, which
are unequally prominent in different cases. The most pro-
nounced, and most constant, is a sense of movement in the
patient himself — to one side, backwards or forwards, up or
down, or a sense of oscillatjon. Nest in frequency is an
apparent movement of objects at which he is looking : these
may seem to move in the same direction ae that in which the
patient seems to move, or in the opposite direction. The
third is less common than the others — an actual movement
in the patient ; it is usually a fall, or a visible tendency to
fall : the fall is commonly in the same direction as the sub-
jective sense of movement, but sometimes it is in the opposite
direction. It is of great importance to ascertain, as exactly
as possible, the precise character of each of these elements.
Although we cannot, as yet, use all these facts in practical
diagnosis, they enable us to understand something of the
nature of the s^Tiiptom, and wUl probably, in the future,
teach us much of its mode of production.

The first significant fact is that the patient usually falls, if
he does fall, in the direction in which he feels a tendency to
fall. At first sight this may seem natural, even necessary ;
but the fact makes it probable that the sensation of vertigo
is really (as Dr. Hughlings- Jackson has suggested) a motor
sensation, the efPect on the sensorium of motor processes,
which, in greater intensity, cause an actual movement.

VERTIGO. 147

I told you that objects sometimes seem to move in the
same direction as the patient, sometimes in the opposite
direction. This difference is not very easy to explain.
It has been thought that stationary objects should appear to
move in the opposite direction to the subjective sense of
movement, because, if the eyes move, say to one side, objects
will pass across the field of vision towards the other side.
Thus, if you move your eyes to the right, an object that was
before in the middle of the field will pass to its left side.
But our sense of the movement of visible objects does not
depend only on their position, or change of position, in the
field of vision ; it depends on this, combined with the con-
sciousness of our own condition of rest or movement. If, for
instance, we remain still, and an object remains in the same
part of the field, we conclude that it is stationary, by a process
of imconscious inference, if the term may be allowed. But if
an object remains in the same part of the field while our
eyes are being moved to the right, we know that it is moving
to the right. It is the same if the head or body is turned
instead of the eyes. Hence, if we have, in vertigo, a sense of
movement without actual movement, an object that remains
in one part of the field seems to move in the direction of the
sense of movement. When an actual movement occurs, this
is probably always far slighter than the sense of movement ;
and the reverse movement of objects in the field, due to the
actual movement of the eyes, may be insufficient to com-
pensate for the greater sense of movement ; so that they still
appear to move in the same direction, although, if the patient
could analyse his feelings in what is usually a moment of
supreme confusion, the objects would probably seem to move
less rapidly than himself. We cannot at present give an ex-
planation of the apparent movement of objects in the opposite
direction to the sense of movement of the patient. It is
probable, however, that the motor and sensory relations, dis-
turbance of which causes vertigo, are extremely complex and
numerous, extending through almost all grades of motor and
sensory cerebral processes, from low to high, and may be de-
ranged at various functional levels. It may be that in certain

L 2

148 LECTURE XI.

derangements the sense of movement, even if it is attended hj
actual movement, does not involve visual impressions in the
resulting error of judgment. Again, the tendency to move-
ment may cause a compensatory and opposite action of the
centres to preserve equilibrium, and this may, in some cases,
exceed its cause. But I will not take you farther into the
obsciirity in which this part of the Buhject is involved.

The centrifugal impulses that maintain equilibrium axe
regidated by certain centripetal impulses that give guiding
lEif ormation regarding the relation of the body to its environ-
ment. Ono class of these consists of the various sensory impres-
sions from the parts on which the body is resting, and of the
impressions from the muscles that maintain the body in its
posture (or the sense of the innervation bestowed on these
muscles). A second is derived from the innervation of
the oculai' mu^les, and from those of the bead and neck.
From this, as we have before seen (p. 85), we derive, uncon-
sciously, our perception of the relation of our body to seen
objects. A thii'd consists of the impressions derived from
the semicircular canals — impressions that vary according
to the pressure of the eudolymph in the ampuUjB of the
canals, under the influence of gravitation and movement. If
any one of these impressions is suddenly deranged, vertigo
results. The most effective is the derangement of that derived
from the ocular and aural sources of information ; and the
residting derangement constitutes, respectively, ocular and
aural (or labyrinthine) vertigo. The same symptom may be
also produced by a very different meohanism, disturbance of
the stomach.

It would be foreign to my present task to describe to you
in detail all these varieties of vertigo. I mention them to
you, because the symptom results from these causes far more
frequently than it does from central disease, and you cannot
ascribe it to the latter until you have excluded a peripheral
origin. Evidence of such origin is afforded by other symp-
toms of derangement of the organs concerned in its produc-
tion, and for these you must search. In ocular vertigo there
is diplopia ; in aural vert-igo there is commonly the "nervous

he "nervous i

J

VERTIGO. 149

deafness " of which I described the symptoms in a previous
lecture (p. 95), and there is often also a noise in the ear.
In gastric vertigo there are other symptoms of stomach dis-
turbance. GKddiness occurs also, but usually in vague form,
in anaemia, and other states of nervous weakness. It is
sometimes met with when no cause for it can be discovered —
a form which, to conceal our ignorance of its nature, has been
termed "essential vertigo." Definite vertigo, in which the
sense of movement is well marked, is far more frequently due
to disease of the semicircular canals than to any other cause ;
and when it does result from any other cause, as, for instance,
from stomach disturbance, you will often find some deafness or
other indication of an affection of the ear, — as if the impair-
ment of the auditory nerve had given a more definite character
to vertigo that was excited by another mechanism. A gentle-
man, a member of our own profession, has suffered all his life
from prostrating attacks of dyspepsia. Some years ago, he
became deaf from labyrinthine disease; ever since, his attacks
of dyspepsia have been accompanied by severe vertigo, from
which he never suffered until he became deaf. The paroxysms
of auditory vertigo may be very severe, and are often ascribed
to some brain lesion. For this reason they may excite con-
siderable, but groimdless, alarm.

Another form of vertigo that may give rise to diagnostic
difficulty is that of epilepsy. Vertigo is a frequent warning
of the minor seizures, and sometimes of the severe attacks.
The almost invariable concurrence of loss of consciousness
sufficiently distinguishes this from the vertigo of peripheral
origin. Remember, however, that this warning is not con-
fined to idiopathic epilepsy. The convulsive seizures that
result from organic brain-disease are often heralded by
vertigo. I have already described the diagnosis between the
two.

Severe vertigo, whatever its origin, is usually attended by
vomiting. There must be a close connection between the
pneumogastric centre and the nerves or centres that regulate
equilibrium. The auditory and vagus nuclei are not far apart
in the medulla, but we do not know whether the connec-

150 LECTURE XI.

tion "between the two is estabUshed there or in the oerebt
The latter is not improbable. A connection certainly exists,
and enables us to understand that stomacb-diBturbance may
produce, and intensify, vertigo, as well as that vertigo may
cause vomiting. Sea-sickness is not improbably produced by
the oscillations of the endolyraph in the semicircular canals.

Diseases of varions parts of the brain, and lesions of various
kinds, may produce vertigo, and it has therefore in itself Httle
diagnostic significance. It is produced by chronic irritating
disease, but rarely by stationary lesions. It occurs at the
onset of acute lesions. The most intense vertigo, however, is
caused by lesions of the middle peduncle of the cerebellum,
and it may then be accompanied by its true motor form, a
forced rotation.

Vomiting is occasionally a most important symptom of cere-
bral disease, but it is a symptom that derives its significance
chiefly from its associations. It has, indeed, certain character-
istics, but these, which are chiefly negative, are common to the
vomiting of functional nervous disorder and of organic disease.
The act of vomiting is reflex, effected through a centre in the
medulla, probably part of the vagus centre. It may be pro-
duced by an undue impression on the nerve-endings in the
stomach — an impression that is felt as pain, discomfort, or
nausea. Suoh is the vomiting of gastric origin, as that of
ulcer of the stomach, or of simple indigestion. But vomiting
may also occur from exalted irritability of the centre ; and, in
this condition, stimulation of the nerves of the stomach by the
mere presence of food may be sufficient to excite the irritable
centre. Such is the vomiting of hysteria, in which food is
rejected as soon as it enters the stomach ; and such is the
vomiting of cerebral disease. The increased irritability of the
centre may be so great that vomiting may occur without any
peripheral irritation, when the stomach is empty.

Nausea may or may not attend this increased reflex excita-
bility. In hysterical vomiting it is generally absent, and it is
often absent in the vomiting of organic cerebral disease. We

VOMITING. 151

know very little about nausea. It is an effect on the sensorium
of the nervous irritation that excites vomiting, but is, as it
were, a collateral disturbance, and is not due simply to the
action of the reflex centre, since vomiting may occur without
it. It is referred as much to the fauces as to the stomach, and
is prominent when vomiting is excited by tickling the fauces,
and when the excitability of the centre is augmented by some
other peripheral irritation, as that of the uterus. Hence, while
its absence suggests, its presence is compatible with, a central
cause.

Organic disease in any part of the brain will cause vomit-
ing, and it is therefore probable that the higher central rela-
tions of the pneumogastric nerve are very extensive — a fact
that is also suggested by the varied functional disturbance of
the cerebral centres that may result from gastric disturbance,
and by the singular readiness with which vomiting may be ex-
cited by olfactory impressions and by some psychical influences.
You may perhaps know Weir Mitchell's story of the man who
was so much disgusted by his wife's vomiting during her first
pregnancy, that he vomited too ; and ever after, when his wife
became pregnant, he became sick. Although vomiting may be
produced by disease in any situation, it is caused with especial
readiness by disease of the pons and medulla, and most readily
of all by disease of the cerebellum. It has been thought that
this is due simply to pressure on the subjacent medulla,
but it is probable that a functional mechanism is concerned
in the effect. Of all the pathological relations of vomiting,
the most remarkable is its relation to vertigo. Of this
relation I have already spoken, and will only further remark
that this association, coupled with the curious disturbance
of equilibrium that results from disease of the cerebellum,
suggests that the vomiting of cerebellar disease is due to an
intimate relation between the gastric centre and this part of
the brain.

Cerebral vomiting results chiefly from irritating disease.
It is rarely due to a stationary lesion. Meningitis, tumour,
abscess cause it; acute lesions only at their onset, or
during the period of secondary irritation. There are two

152 LECTURE XI.

facts regarding cerebral vomiting that I would impress upon
you. The diseases that cause vomiting usually cause also
pain in the head, and the vomiting often attends paroxysms
of pain, and adds much to their significance. They give a
similar significance to pain that is slight, and would not, in
itself, suggest organic disease. The second fact is that brain
disease, which exalts the excitability of the gastric centre,
does so gradually, and the vomiting may be at first excited
by a peripheral cause — a cause that might not be effective
were it not for the exalted excitability of the centre. In such
cases the exciting cause may be accepted too readily as an
adequate explanation. This caution is especially necessary in
the case of children. I have more than once known the
vomiting of meningitis or of cerebral timiour to be, at first,
excited by some injudicious food, and to be therefore thought
to be of no importance, until graver symptoms gave signifi-
cance to it. Remember that indigestion, sufficient, by itself,
to make children vomit, usually makes them ill ; and if a
child vomits food without seeming otherwise indisposed, do
not at once assume that there is nothing more the matter
with it than indigestion, but watch it carefully.

LECTUEE XII.

SYMPTOMS (CoTUiniied) : TEMPERATURE— PULSE— DISTURBANCE
OF RESPIRATORY, DIGESTIVE, AND URINARY ORGANS-
SYMPTOMS OBSERVED WITH THE OPHTHALMOSCOPE.

Gentlemen, — ^We have to consider to-day a miscellaneous
group of symptoms that are sometimes described as being
"outside the nervous system," apparently because they are
within the range of other organic systems. They are no more
" outside the nervous system " than is paralysis of the arm.
We will begin with the changes in the heat of the body
that are produced by brain disease.

Elevation of temperature accompanies many diseases of the
brain. The relation between the two varies in different cases.
In some the pyrexia is simply associated, the result of the cause
of the cerebral disease. In others it is the result of the patho-
logical process in the brain. In others, again, it is the result of
the lesion, and not of the process that causes the lesion. In
each case it is necessary to recognize the precise relation, in
order to estimate correctly the significance of the pyrexia.
Instances of the first form are presented by the fever that
accompanies embolism in a case of ulcerative endocarditis,
or a secondary abscess, due to septicaemia. In these cases the
pyrexia is chiefly due to the general disease, and is simply
associated with the cerebral lesion. The second relation ob-
tains in most cases of intracranial inflammation. The morbid
process raises the temperature, as it would if it occupied any

184 LECTURE XII.

other situation. The pyrexia of meningitis, and the eleyation
of temperature that occurs a few days after an acute lesion,
are instances of this form. These two causes of pyrexia often
concur ; a general disease causing fever produces a cerebral
lesion that has a siTailar effect. The fever that results from
an intracranial cause varies in its degree and course much
more than does that which results from a similar process
outeide the nervous system. Two facts are especially im-
portant. Pyrexia may be absent with an inflammation that
elsewhere would certainly raise the temperature. Apparently
this is the effect of a restraining influence exerted by the
irritated nervous system. This influence may even go so far
as to lower the temperature under the normal, in spite of the
process of inflammation. The second fact is that the rise io the
pulse-rate which usually attends fever may, in like manner, be
restrained, and this, even though the rise in the temperature
is not prevented. The pulse may even be lowered to an
abnormal iofrequency. Thus a nonnal temperatiu-e does not
exclude inflammation; and elevation of temperature, if it
occurs, derives additional significance from an infi'equent
pulse.

The third relation between brain disease and temperature
is very remarkable. Lesions iu the pons or medulla may cause
a very rapid elevation of temperature, which, in the course
of an hour, may attain a height of 106°, 108°, or 110°.
This hyperpyrexia is usually associated with copious perspira-
tion. It occurs not only in various acute lesions, but
sometimes in the course of chronic lesions. It may also
result, although very rarely, from more extensive disease,
such as meningitis, probably from an influence exerted
on the lower parts of the brain. This hyperpyrexia is
apparently due to the loss of action of some influence that
normally restrains the heat-producing mechanisms of the
body. As you may know, a similar effect follows experi-
mental lesions in this part of the brain in animals. It is
always of very grave significance, usually being followed by
death within a few hours.

There are one or two miscellaneous facts regoi-ding the

TEMPERATURE. 155

temperature in diseases of the brain and nervous system mth
which you should be acquainted, in order to avoid errors into
which you might otherwise faU. When convulsions succeed
one another with great frequency — ^the " status epilepticus "
— ^the temperature often rises steadily, and may attain an
alarming height — 106° or 108°. The rise is the result of the
convulsions, and does not indicate any inflammatory condition
of the brain. If the patient does not die, the temperature
slowly subsides as the convulsions become less frequent.
Some degenerative diseases, as general paralysis of the insane,
are occasionally attended with slight chronic pyrexia, which
appears to have its origin in the nervous system, and does not
necessarily indicate any inflammatory condition. In the same
class of diseases, paroxysmal disturbances occur, characterized
by great heat of the skin, often sweating, sometimes loss of
consciousness, sometimes convulsions. The patient may seem
for a few hours in a most grave condition, as if some acute
inflammation had suddenly- developed ; but in a few hours
more all these symptoms have passed away. These are called
"congestive attacks"; we do not know their real nature,
or whether the indications of congestion are primary or
secondary. Thirdly, children are sometimes liable to attacks,
probably of the nature of migraine, in which there are
severe headache, fever, and, sometimes vomiting. The con-
dition of the child resembles that of one suffering from
meningitis, but the symptoms develope more rapidly than
those of meningitis, reaching their height in a few hours
from the onset. They pass away with equal rapidity. Such
attacks may recur at intervals of a few weeks or months.
The rapidity of the onset, and the history of previous attacks
of the same character, distinguish them from more serious
affections. Their recognition is important, otherwise you
may make a diagnosis of fatal disease, and the patient may
be well at your next visit.

Depression of temperature occurs at the onset of some acute
lesions, especially haemorrhage, and in some chronic diseases
in which there is profound lethargy, and all the bodily func-
tions are lowered, in response to the lowered function of the

156 LEtTUBE Xll.

brain. In meningiiis, the influence that prevents an ele
tion of the temperature may, as I have aheady mentioned,
go so far as to reduce it below the normal, in spite of the
inflammation.

Many diseaaea of the brain have no special influence on
the pulae. The most important fact is that which I have
already mentioned, that the frequency of the heart's action
may not be increased, and may even be lessened, by morbid
processes that elsewhere would increase the pulse-rate. In
inflammation, variations in frequency occur without any
recognizable condition to which they can be attributed, and
irregularity in rhythm is occasionally a marked and early
symptom. Infrequency is not uncommon in chronic disease,
and also at the onset of sudden lesions. When the latter ore
in the neighbourhood of the medulla, there may he great
irregularity in both frequency and force.

Vafio-raotor disturbance occurs as part of hemiplegic
palsy, and this form has been already described. In
meningitis there is often a strong tendency to trophic dis-
turbance in the skin — bed-sores and the like — similar
to that which occurs in hemiplegia, and occasionally
this symptom has a diagnostic value. I have known, for
instance, the readiness with which blisters were caused
by a hot-water bottle to first arouse a suspicion of the
grave nature of an illness that had been regarded as
hysteria. Dilatation of the cutaneous vessels, excited by an
irritation of the skin {such as a stroke with the finger-nail),
lasts long in many cases of acute brain disease, and much
significance was formerly attached to the " tache cerebrale,"
as the red line thus produced was called. But it oqeora
also in many general diseases, and is as likely to mislead
as to aid the diagnosis.

Respiration may be either quickened or slowed by
cerebral disease; hut the change is considerable only when
the functions of the brain are impaired by extensive dis-
ease, such as a large hsemoirhage, or when the lesion is in

the lesion is in 11

RESPIRATION — ^DIGESTION THE URINE. 157

the neighbourhood of the respiratory centre, Le,^ is in
the pons or the medulla. Under these circumstances the
respirations are sometimes very irregular, and there is
occasionally a peculiar respiratory convulsion, a prolonged
convulsive cough, or a hiccough. The rhythmical varia-
tions that constitute the " Cheyne-Stokes " breathing (see
p. 110) occur towards the end of many cerebral diseases,
such as cerebral haemorrhage or meningitis. In some rare
cases of disease of the pons or medulla, in which conscious-
ness has been preserved, there has been intense subjective
dyspnoea.

In coma, the respirations are often quickened, not as a
direct result of the cerebral lesion, but in consequence of
the accumulation of mucus in the air-passages. This is
due chiefly to respiratory inertia, but in some cases neurotic
congestion may increase the secretion, since lesions near
the pneumogastric centre may cause actual haemorrhage into
the substance of the lung.

Of the derangements of the digestive organs, the most
important, vomiting, has been abeady described. Consti-
pation is common in acute and subacute diseases, and some-
times adds weight to the significance of other symptoms.

Alterations in the composition of the urine may be a direct
result of the cerebral lesion, but are rare, and of little dia-
gnostic value. Excessive secretion, and the presence of albu-
men and sugar, have been observed as the result of disease,
acute and chronic, in various parts of the brain, most fre-
quently when the lesion was in the pons. The derangement
has usually been transient ; occasionally, glycosuria has con-
tinued for many months. I need scarcely mention that
organic renal disease, and previous diabetes, must be care-
fully excluded before the change in the urine can be ascribed
to the influence of the cerebral lesion.

The sphincters are affected as frequently in disease of the
brain as in that of the spinal cord, but rarely in the same

158

i-EcrruHE xn.

degree. Both retention of urine and incontinence are met
with, but the iucontinenee is the result of overSow, and uot of
complete inaction of the ephineter. It is very important
to reraemher how often there ia an apparent incontinence
that ia uierely the result of mental inertia. I have mentioned
this tefore, in speaking of the mental changes ; and I told
you how significant it is, as an indication of a profound
degree of mental change — more profound than the other
symptoms might lead you to imagine.

h

I have left to tlie last the changes in the fundus oeuli,
not heeanse they are last in importance, hut because they
stand to the cerebral lesion in a relation somewhat different
fi'om that of the symptoms that have Mtherto engaged our
attention.

The indications of brain disease that are revealed by the
ophthalmoscope are not only of the highest practical im-
portance, hut are of interest as a salient indication of tiie
progress of medical science, since thirty years ago they were
unknown. Morbid appearances in the eye are frequeut
in intracranial disease, and often prove the existence
of such disease when other sjTnptoms are inconclusive, or
afford evidence of its nature that can be obtained from no
other source. For this and other reasons, skill in the use of
the ophthalmoscope, and familiarity with the conditions it
reveals, are indispensable to the physician. I cannot too
strongly impress upon you the importance of acquiring
dexterity in the use of the instrument as early as possible, in
order that you may be able to utilize the opportunities for
g ainin g experience which almost every department of prac-
tical work will supply. These opportunities wlU be lost if
you only learn to use the instnmient when you proceed,
towards the close of your course, to the special study of
diseases of the eye.

Some of the changes in the eye met with in brain disease
are merely associated, the result of, and evidence of the
cause of, the cerebral lesion. Others are consecutive, the

aonseoutive, tne i

OPHTHALMOSCOPIC CHANGES. 159

effect of the brain disease, and evidence of its presence and
of its nature. The associated and consecutive symptoms are
sometimes conjoined.

The associated changes are due to the constitutional condi-
tion on which the brain disease ultimately depends. The most
important of these are the following : First, albuminuric re-
tinitis, acute or chronic, associated chiefly with arterial degener-
ation, such as causes cerebral haemorrhage or cerebral softening.
Secondly, syphilitic disease, especially choroiditis, orchoroiditic
atrophy, associated with lesions of the brain due to acquired or
inherited sypMKs. Thirdly, tubercular diBoase-tubercles of
the choroid occasionally in tubercular meningitis, very rarely
massive tubercle in cases of tubercular growths in the brain.
Other forms of associated growth are tpo rare to be of prac-
tical importance. Fourthly, vascular lesions of the retina
sometimes coincide with similar lesions in the brain. Thus,
embolism of the central artery of the retina may occur in the
same patient, and even at the same time, as embolism of a
cerebral artery. Miliary aneurisms on the retinal arteries
have been observed to coincide with cerebral haemorrhage due
to similar aneurisms in the brain. They are, however, ex-
tremely rare. Haemorrhages in the retina are more common,
and are of some significance. They occur especially in
albuminuria, in gout that has profoundly affected the system,
in leucocythaemia, profound anaemia, purpura, ulcerative
endocarditis, and other forms of septicaemia. In the latter
they have often white spots in the centre, and are the result
of capillary septic embolism. Haemorrhages, identical in
aspect, are sometimes found in the same cases in the cerebral
meninges.

The consecutive changes, that are the result of the cerebral
disease, comprehend optic neuritis and atrophy. Neuritis or
papillitis consists in swelling and increased vascularity of the
intra-ocular termination of the optic nerve — ^the " optic papilla."
It will be remembered that the end of the nerve is visible in
the fundus as the " optic disc," the boundary of which is the
oval opening in the sclerotic and choroid. The fibres radiate
from the nerve on all sides, but not equally ; they are few on

tlie temporal side. The nerve-elementa are so translucent
that they do not obseure the edge of the disc, except in some
cases and to a slight extent, above and below, where they are
more numerous. The disc is rarely uniform iu its sui'face,
because the separation of the nerve-fibres leaves a central
hollow — the " physiological cup " — in which there are few or
no vessels, and which is therefore pale, while the periphery
of the disc has a rosy tint from the minute vessels that lie
among the nerve-fibres. This physiological cup varies much
in size, and may be absent. The vascular portion of the disc
also varies in extent (inversely as the cup), and varies so
much in tint that no inference can be drawn from its colour
unless this is observed to change from time to time. Mere
congestion, therefore, consisting only of increased vascularity
of the disc, is very difficult to recognize, and, although it
probably occurs, it is extremely rare as an isolated condition,
and is of small practical importance. An actual pathological
change, however sHght in degree, is usually attended by some
swelling of the papUla, and espeoially by lessened trans-
parency of its structures. The effect of this change is first
to lessen the sharpness of the edge of the disc, and then to
obscure it altogether. It is, therefore, to this point, the
sharpness of the edge, that attention must chiefly be
directed. The effect of a morbid change on the edge of the
disc is greater when the examination is made by the direct
than by the indirect method. On the other hand, if the
indistinctness is apparent, and not real — is dne to the tint of
the disc being nearly that of the adjacent choroid, and not to
the lessened transparency of the structures in front of it — tlie
edge is more distinct by the direct than by the indirect method
of examination. In the early stage of neuritis the edge of
the disc, seen by the indii-ect method, may appear a little
blurred, and surrounded by a pale halo, while by the direct
method the halo is resolved into a striated, semi-opaque
layer, completely concealing the edge. The early change is
greatest on the nasal side, which may be obscured when the
temporal edge of the disc, on which there are few nerve-fibres,
is still sharp. As the change advances, it involves the whole

OPHTHALMOSCOPIC CHANGES. 161

circmnf erence of the disc, and the swelling rapidly encroaches
on, and ultimately obliterates, the normal white depression
in the centre of the disc. The prominence of the swelling
is readily recognized by the relative displacement that the
different parts appear to undergo on a lateral movement of
the observer's head in the direct, or of the lens in the indirect,
method of examination. It is also shown by the loss of the
central reflection from the vessels where they course down the
sides of the swelling, and their plane is no longer at right angles
to the line of vision. The tint of the swollen papilla becomes
a full red, or, more commonly, a greyish-red, on indirect
examination, but the direct method shows a fine striated
vascularity. As the prominence increases, the swelling becomes
wider in extent, until it may be two or three times the diameter
of the normal disc. White spots may appear on its surface,
due to the accumulation of products of degeneration. At
first the retinal vessels present little change in size, but as the
swelling increases, their compression causes the veins to become
broader, and the arteries narrower, and extravasations of
blood may be visible on the surface or margins of the swollen
area. The process varies much in the rapidity with which it
is developed ; it may reach a considerable intensity in a fort-
night, or be still moderate in degree at the end of three or
four months. As a rule, the more quickly it is developed, the
more intense it becomes. Retrogression is indicated by a
diminution in the vascularity, still greater contraction of the
arteries, and, later on, contraction of the veins also, if the
degree of neuritis has been considerable. The swelling re-
mains, for some time, pale and soft-edged, and slowly sinks
until the edges of the disc appear. The substance of the disc
is for long, often permanently, occupied by new tissue,
which, with the narrowed arteries, affords evidence of the
preceding inflanmiation. Other indications of this are often
to be seen in damage to the adjacent edge of the choroid. It
is only when the neuritis has been slight that the disc resumes
a perfectly normal aspect. When much new tissue has been
formed, this, by its cicatricial changes, leaves the disc white
and atrophied, in the condition of "consecutive atrophy," or

M

" nemitio (papillitic) atrophy," as it is also termed. When
the papillitis has been very intense, and the swelling wide in
area, the adjacent retina may suffer in its nutrition, and pro-
dnctB of degeneration may remain as white spots, espeeiaUy
near the macula lutea, simulating the aapect of albumiuimc
retinitis. The microscope reveals, in the substance of the
swollen papilla, various inflammatory changes, of which you
will find details and illuatrations in my work on "Medical
Ophthalmoscopy." Similar, although slighter, changes may
he traced back in the substance of the optic ner^'es, or in their
aheatha, even to the chiasma, and they may be more intense
in front of the chiaama than they are midway between this
and the eye. The outer sheath of the optic nerve in
most cases is distended by Hquid, so as to form a pyriform
swelling behiud the globe. The space within this sheath is
continuous, behind, with the subaiuchnoid space around the
brain, and in front, with the Ijonphatic spaces in the optic
papilla.

A shght and even considerable degree of optio neuritis may
cause UD sj-mptoms; acuity of vision may be imimpaired,
colour-vision normal, the visual fields unrestricted ; but when
intense, sight suffers in each of these characters, and may be
entirely lost. The damage to vision is often greater during
the stage of subsidence than it is during the active period of
inflammation, probably because the nerve-fihres are eom-
jiressed by the cicatricial contraction of the tissue-elements
formed during the inflammatiou. As I mentioned in a
preiiouB lecture (p. 73), the affection of sight ia not neces-
sarily due to ihe visible papillitis ; it may be the result of more
intense inflammation behind the eye, or the effect of the
intraoranial disease. After the neuritis has quite subsided,
improvement in sight often takes place by the recovery of
some of the damaged fibres, but there may remain absolute
blindness, or considerable amblyopia, and often there are
very irregular changes hi the field of vision, both for white
and colours.

Optio neuritis may result from many diseases of the brain,
hut the most frequent cause is tumour, and a considerable

OPHTHALMOSCOPIC CHANGES. 163

degree of neuritis is seldom due to any other lesion. Next
in causal frequency is meningitis, especially when it affects
the base of the brain ; the inflammation caused by meningitis
is usually less intense than that of tumour, perhaps on account
of the briefer duration of the disease. Optic neuritis does not
result from cerebral haemorrhage, or from thrombotic soften-
ing. It has been several times observed in cases of softening
from embolism, when the source of the obstructing plug was
active endocarditis, perhaps because the material carried from
the valves is of an irritating, septic character, and determines
a greater degree of secondary inflammation in the softening
produced. Neuritis has also been met with, once or twice, in
eases in which no naked-eye lesion of the brain could be found,
but in which the microscope revealed slight inflammatory
changes — a diffuse cerebritis. In all these cases the neuritis is,
as a rule, double, although it may develope more rapidly in
one eye than in the other. Occasionally it is one-sided, and
then it is generally on the side opposite to the lesion; but
unilateral optic neuritis is much more frequently due to disease
at the back of the orbit, or at the optic foramen.

It must be remembered, however, that optic neuritis may
result from other causes than intracranial disease ; it occurs
in chlorosis, albuminuria, lead-poisoning, and after certain
fevers, especially scarlet fever and typhoid. An important
fact is that in many of these conditions its occurrence is
associated with some cerebral symptoms ; thus, when neuritis
preponderates over the other retinal changes in albuminuria,
there is usually much pain in the head, and in lead-poisoning
it is usually associated with the acute cerebral symptoms that
have received the name of " encephalopathia satumina."
Remember this concurrence of cerebral symptoms with
neuritis due to a general disease, because it often gives rise to
a diagnostic difficulty.

The mechanism by which optic neuritis is produced is a
subject on which various opinions have been held. A full
account of these wiU be found in "Medical Ophthalmoscopy."*
It is sufficient here to say that the early theory that neuritis

* Second Ed., p. 65.

M 2

p

164 LECTURE XII.

is due to increased iEtracramEil pressure, acting mechanically,
has been proved erroneous. Slow increase of intracranial
pressure has aknost no influence on the occurrence of this
symptom. In a large number of cases of neuritis there is
distinct evidence of a descending inflammation, either along
the trunk of the optic nerve, or along ita sheath ; and in cases
of meningitis, such descending inflammation is invariable.
The distension of the optic sheath with serum has been re-
garded as the chief mechanism, but it is not essential for
the production of neuritis ; it may be absent, and its occur-
rence is related especially to the presence of an excess of sub-
arachnoid fluid. The signs of mechanical "strangulation,"
which are to be observed in cases of intense neuritis, are no
evidence that the inflammation was caused by any mechanical
process. The cause of the strangulation is the compression of
the veins by the inflammatory products within the swollen
papilla, and not, as was once thought, their compression within
the sclerotic ring or behind it by the distension of the sheath.
It is probable that optic neuritis is rarely due to a single factor,
and that the most potent element is the descent of a process of
tissue-irritation, which, when it reaches the papilla, sets up a
more intense inflammation ; that in some cases this influence
is alone effective ; and that in others it is aided by the
distension of the sheath, which hinders the escape of effete
products, increases asdema, or even conveys irritating mate-
rial. The distinction between optic neuritis and " choked
disc " is one of degree, and not of mechanism. So far as
optic neuritis has any single significance, it is that of an
irritative process within the skull.

There is an impoi-tant relation between the chronieity of
the neuritis and that of the intracranial process. A chronic
cerebral process may cause an acute neuritis, but a Ghronio
neuritis never results from an acute process, and the degree of
the chronieity of the neuritis is an indication of the degree of
chronieity of the intracranial disease. When the latter begins
to improve, the neuritis lessens, and the commencing sub-
sidence of the intra-ocular inflammation is often the first
indication of the improvement of the brain lesion.

P HTH A I, MOSIOP 1 f CHANGES.

165

Optic nerve atrophy is a less frequent symptom of brain
disease than is optio neuritia, with the exception of that form
of atrophy ■which is the consequence and evidence of past
inflammation. Primary atrophy is rare, and confined to those
forms of hrain disease that are degenerative in nature. It is
met with, for instance, in cases of disseminated sclerosis, and
of general paralysis of the insane, as an associated sjinptom.
Secondary atrophy occurs, not infrequently, in consequence
of damage to the optic nerve behind the eye, or to the optic
chiasma. Disease of the optic tract does not cause marked
atrophy of the disc, when the disease is at the ehiasma, both
eyes may suffer ; when it is in front of the ehiasma, the atrophy
is usually limited to one eye. The cbaxacteristic of secondary
atrophy is that sight fails without ophthabnoscopio changes to
account for the failure, and this is slowly followed by atrophy.
The only distinctive features of the failure occur when the
disease is at the ehiasma (see p. 73), If the lesion of tbe
nerve is inflammatory, some descending inflammation may
reach the eye and be visible at the optic disc. Its amount
depends on the intensity of the inflammation, and on its
proximity to the eye, but it is always insufficient to account
for the affection of vision. When the lesion is near the eye,
the vessels often present distinct constriction. Of the signifi-
cance of these various changes as indications of the patho-
logical nature of tbe cerebral lesion, I shall have more to say
when this problem engages our special attention.

You may have observed that, in this outline of tbe changes
met with in brain disease, I have said nothing about conges-
tion or anoemia of the retinal vessels or of the disc, as an
indication of similar states of the brain. Exaggerated
expectations and, indeed, opinions were formed, when the
ophthalmoscope was first introduced, regarding its revela-
tions. It was thought that, since the blood comes to the eye
from a cerebral artery, and returns to an intracranial sinus,
the circulation in the eye would share, and show, the changes
in that of the brain. But experience has not confirmed the
opinion. The circulation in the eye is, so to speak, auto-
nomous ; the state of the vessels is regulated by independent

i

166 LECTURE Xll.

influences. When all the veins of the head become over-
distended, in consequence of an obstruction to the flow
through the superior vena cava, the retinal veins suffer far
less than those on the surface of the head, no doubt because,
in the closed chamber of the eye, neither distension nor
contraction of the vessels can readily occur from a mechanical
cause. The information afforded by the ophthahnoscope is
important and extensive beyond the dreams of its inventors,
but the expectation that was most confidently held has not
been fulfilled; and if you find any author professing to
diagnose the state of the cerebral circulation from that of
the eye, or drawing therefrom indications for treatment,
you may safely conclude that he knows very little about
the subject.

LECTUEE XIII.

DIAGNOSIS OF THE SEAT OF DISEASE: " LOCALIZATION "-
GENERAL METHOD OF DIAGNOSIS — CEREBRAL HEMI-
SPHERE, CRUS, THE CORPORA QUADRIGEMINA.

Gentlemen, — ^According to the loose use of words^ that is
still oonunon in medical terminology, we are said to "localize"
disease, that is, to make it local, when we infer its locality
from the symptoms it produces ; and this process of inference
is termed " localization." In the previous lectures we have
considered the chief symptoms of brain disease, and we have
learned in what part of the brain a lesion may be situated to
produce those symptoms. It is necessary now to review these
facts from the other side ; to look at the symptoms from the
standpoint of brain-regions. Before we do so, I must remind
you of the distinction between the direct and indirect effects
of disease (see p. 48), and that only those symptoms which
last for some time can be regarded as due to the destruction
wrought by the morbid process. Moreover, you must bear in
mind that the nature of a lesion, as well as its position, exerts
an influence on the character of the symptoms that are pro-
duced. Speaking generally, we may say that in acute lesions
the symptoms are, at first, wider in range, while in chronic
lesions they are, throughout, slighter in degree, than might be
anticipated from our knowledge of the function of the parts
that are implicated. Moreover, the symptoms produced by

168 LECTURE XTII.

slow proceBses, Bueh as a growth or an abscess, differ in
range, according ae the disease influences the grey or the
white subatanee, nerve-cells or nerve-fibres. The fibres are
strangely tolerant of slow pressure, especially when this is
widely diffused. A tumoiu' or an abscess may occupy the
position of the motor path, and yet cause only slight palsy,
because the fibres have been merely displaced by it, and still
retain much power of conducting, in spite of their compression.
When auch a disease occupies the grey matter, there is a
similar, although slighter, tolerance of pressure, so far as
ooneems loss of function, but the neiTC-cells exposed to the
morbid influence are in a state of abnormal irritability, and
the connection between the nerve-cells of the cortex is bo
abimdant and extensive, that the functional change may spread
over a wide area and to a considerable distance from the
primary disease. Discharges, causing convulsions, may com-
mence at various parts of the area thus exalted in irritability.
Moreover, centres are sometimes inhibited by the irritation,
instead of being "discharged"; and there restilta loss of
function instead of over-action. Hence, the symptoms produced
by such diseases are often anomalous, and extreme care is
needed in drawing conclusions from them. Some extensive
collections of facts relative to this subject have been rendered
absolutely valueless by disregard of this consideration.

To return to our immediate subject. Having ascertained
what symptoms are present, we must, in the case of an acute
lesion, endeavour to distingnish the direct from the indirect.
We can only do this with certainty by waiting till the in-
direct symptoms have passed away, as they will have done
in a few weeks. We may, indeed, moke a guess at the direct
symptoms soon after the onset, from their severity, and
from the absence of any indication of early improvement
ill tliem ; but to attain a high degree of probability in oiu:
local diagnosis we must, in many cases, wait. Fortunately
we have uot thus to wait for indications of the nature of
the lesion, on which, and not on the exact seat of the
disease, our treatment depends.

LOCAL DLiGNOSlS. 169

Before you can draw any conclusion from the symptoms
as to the seat of the disease, you must consider their mode
of development, whether slow or sudden, simultaneous or
successive. The bearing of this on the problem we are now
considering is very important. If the morbid process is
one of sudden onset, only those symptoms that came on
together can be regarded as due to the same lesion. Take,
for example, a not imcommon case, that of a patient who
presents paralysis of the limbs on one side, and of the
third nerve on the other. These are symptoms of
disease of the cms. But to have this significance, if
the hemiplegia came on suddenly, the paralysis of the
third nerve must have come on at the same time. If you
find, on inquiiy. that the paralysis of the third nerve
existed before the sudden hemiplegia, it cannot be due
to the same morbid process, and the affection of the third
nerve must be eliminated from the problem of the seat of
the disease causing the hemiplegia. But if both were
gradual in development, we cannot certainly dissociate them :
they may then be due to one lesion or to separate lesions.

Having thus determined what symptoms developed in such
a manner that they may possibly be due to a single lesion,
we have next to ask. Is there any part of the brain in which
a single lesion would produce this group of symptoms?
Some combinations of symptoms can be caused only by a
lesion in one situation ; others may be produced by a lesion
in any one of several places. Others, again, are of such
a character that there is no part of the brain in which a
single lesion will produce them. To return to the instance
we have just taken, hemiplegia on one side, and paralysis
of the third nerve on the other, can be produced only by
a lesion of the cms. Hemiplegia and paralysis of the third
nerve on the same side cannot be caused by a single lesion
in any situation, since the motor tract, where contiguous
to the nerve, is that to the limbs of the opposite side.

Many of the symptoms of brain disease are of no localizing
value, because they may be caused by disease in any
situation ; while others are of low value, because, although

170 LE<,TUHI-; XIII.

produced by disease in various places, they are rather more
frequent when it occupies certain situations. Most of the
diffuse symptoms (see p. 49) are of this character — head-
ache, vomiting, optio neuritis, mental change, loss of con-
sciousness. In so far as these vary with the seat of the
disease, their variations have been mentioned in the account
of the symptoms. Some syraptoma that are focal, and
not diffuse, are produced by disease in so many places that
they have but little significance, as, for instance, conjugate
deviation of the head and eyes from the paralysed side in
severe hemiplegia. This may occur in lesions of the motor
tract anywhere between the pons and the cortex.

Bearing in mind these facts, we may proceed to our review
of the chief symptoms that arc produced by lesions in vajious
parts of the brain, and we may commence with the ceirhrnl
cortex. In the frontal hhc, or rather what is termed the
prefrontal lobe, in front of the ascending frontal, lesions
are usually unattended by either motor or sensory symp-
toms. Considerable mental change is rather more frequent
than in other situations, sometimes taking the form of
chronic insanity, and gives some support to the opinion
which naeribes to this region a high psychical importance.
But these symptoms are neither characteristic nor invariable.
The posterior paii of the lowest fi'ontal convolution on the
left side constitutes, however, an exception to the negative
character of this region, since disease here, aroimd the
anterior hmb of the fissure of Sylvius, causes, with much
uniformity, motor aphasia. Lesions which irritate, and are
adjacent to the ascending frontal, often cause convulsions
that begin locally. It is possible that the limb-centres ai'e
not always strictly hmited to the ascending frontal and
that disease on the roots of the antero-posterior gyri may
cause motor sjTnptoms in some individuals, and not in others ;
but no SjTnptoms have been observed in man corresponding
to the fmictional centres that you often see marked on these
convolutions in diagrams of the human brain, to which
they have been transferred from the brains of monkeys.

LOUAI. 1)1AGX()S1«. 171

^'central area of the brain (as the motor region-
ascending frontal, ascending parietal, and superior parietal
— ia often termed), disease causes motor paralysis. There is
loBS of power in the leg when the lesion is in the upper third;
loss of power in the arm, when in the middle third ; in
the face, when the disease is in the upper half of the lower
third; in the lips and tongue, when it is in the lowest pait
of the ascending frontal ; and, on the left side, disease in
this pai-t causes also aphasia. Partial hemiplegia is much
more eominon than paralysis involving the whole of
the side, and the pai-ts that suffer together are those for
which the centres are contiguous in the cortex. Convulsions
are exceedingly common, and their charfteteristic feature is
the local commencement, already described, and due to the
commencement of the discharge in an irritated centre. This
ia not always the region most diseased. Conaiderahle disease
in one centre may cause dischaxges to start from an adjacent
centre less diseased, and therefore capable of greater fimc-
tional excitement. Thus a tumour occupying the highest
part of the ascending frontal convolution (leg-centre) caused
at first convulsions beginning in the foot, and afterwards, as
the diseaae advanced, con\-ulsions beginning in the hand (the
centre for which was not invaded by the growth), and even
sometimes in the face (the centre for which was some distance
from the tumoiu-). Thus, also, the disease causing such con-
vulsion may be near, but not in the motor area. Hence local
paralysis is a much more decisive indication of the seat of
the disease than are the local convulsions. In the case of
tumour, with changing convulsions, just mentioned, the leg
became paralysed, and this indicated that it was in the leg-
centre that the destruction of tissue was in progress. Disease
of the motot cortex often causes some defect of sensation,
chiefly in the extremity of the paralysed limb, and in the
convulsions a local sensory aiu-a often precedes the spasm, and
may even pass through the whole side before the spasm comes
on (see p. 62). There is never complete hemiansesthesia when
the disease is Kmited to the motor region. With the cutaneous
defect in the extremity paralysed, and even without this, there

J

172 LECTITKE XIII.

18 usually an inability to recognize the position of tlie limb;
but we do not yet know whether this losa is confined to cortical
lesions. Probably it ia not (see p. 69).

Disease is rarely limited to the remaining part of the
parietal lohe, supra-marginal convolution, and there ia much
uncertainty as to the symptoms produced. The lesion
ufluitlly extends to the motor region, causing hemiplegia,
and there is some reason to think that ptosis accompanies the
hemiplegia rather more frequently when the lower parietal
lobe ia affected. Extensive disease of the outer surface of
the hemisphere causes hemianEestheaia, and to this the
disease of the lower parietal lobe probably contributes.
Defects of speech have been met with, although not with
such constancy or uniformity as to furnish diagnostic indi-
cations. A lesion of the angular gyrus at the infero-
posterior angle of the parietal lobe, probably causes crossed
amblyopia, and disease about this region causes word-blind-
ness; but the precise locality on which this symptom depends
is not yet known. Only one symptom is known to he pro-
duced by disease of the occipital lobe — hemiopia, — and we are
still imcertain as to the exact part of the cortex of the occi-
pital lobe on which the symptom depends. Small lesions may
cause a losa of only part of the half-field, e.g., a quadrantic
defect. It is probable that the separation between the pre-
served and blind halves of the field does not differ from that
in the hemiopia produced by diaeaae in the lower part of the
visual path, but that there is greater peripheral limitation
of the preserved half of the field. Irritating disease of this
region may cause convulsions that commence with a visual aura
referred to the opposite eye or opposite side. Disease of the
teinporo-spheiioidul lobe causes no motor or sensory sympfoms
unless the first temporal convolution ia involved, and then
deafness is produced on the opposite aide ; and if the disease
is on the left side of the brain, there is word-deafness and
sensory aphasia. Irritating disease may cause convulsions
that commence with an auditorj' aiu^. If the lesion is on
the inner surface of the lobe, and involves the anterior part
of the uncinate convolution, it is prohable that loss of smell

LOCAL DIAGNOSIS. 173

may occur on the same side. It is important to remember
that the inner part of this lobe is contiguous to the optic
tract ; tumours are apt to invade the tract, and thus cause
hemiopia, which may be followed by hemiplegia from the
further extension of the disease into the cms cerebri. This
is one of the commonest causes of hemiopia from disease of
the tract.

The island of Reil is rarely the seat of isolated lesions,
and much imcertainty still exists regarding its functions
and the symptoms that result from its damage. Defects of
speech, similar to those that result from disease of the third
frontal convolution, have been attributed to its disease ; but
the evidence is not altogether satisfactory, and speech-defect
has been absent in some cases in which the insula was
extensively damaged.

In the white substance of the hemisphere, centrum ovale,
the symptoms produced by disease resemble, for the most
part, those that are caused by lesions of the corresponding
part of the cortex, with the exception that convulsions are
rare, save in the case of tumours, which cause persistent irri-
tation. The disturbance of speech is transient imless the
disease is seated just beneath the cortex, for the reason given
in a previous lecture (p. 130). Hemiopia results from disease
of the white substance of the occipital lobe, but it is doubtful
whether crossed amblyopia occurs imless the angular gyrus
is affected. Lesions of the white substance of the lower
part of the temporal lobe, and of most of that of the pre-
frontal lobe, cause no symptoms.

In the central ganglia, lesions of either part of the corpus
striatum cause no lasting symptoms if limited to the grey
matter. I have seen the lenticular nucleus softened from one
end to the other, and the patient, before death, presented no
indication of hemiplegia. I will not say that the disease
caused no symptoms, but her history was very carefully taken,
and no account was obtained of any motor or sensory
symptoms. Such cases are, however, extremely rare, because,
in most instances, the internal capsule suffers also. A lesion
of the anterior or middle part of the optic thalamus may also

I.EC'TURK XIII.

cause no symptoniB, although there is some reason to think
that the latter sometimes causes athetoid inco-ordinafinn.
When the posterior portion of the thalamus, the pulwnar,
is diseased, heraiopia occurs ; but it is not quite eei-tain
whether it depends on such disease, or whether there is, in
these cases, interference with the posterior portion of the
optic tract, which enters the corpus geniculatimi close to
the posterior extremity of the thalamus. The balance of
evidence, however, is in favour of the dependence of the
symptom on the disease of the thalamus.

The effects of disease of the iiifemtil mpmk vary according
to the part damaged. When this is the anterior limb,
between the caudate and lenticular nuclei, no symptoms
result. Disease of the anterior two-thirds of the hinder limb
causes hemiplegia of the ordinary type, and is indeed the
most frequent cause of this. It is supplied by branches of
the middle cerebral that are apt to be occluded, either from
disease of the wall of the vessel, or from embolism, and the
arteries adjacentrupturemorefrequently than any other, caus-
ing hsemorrhage, which tears across the fibres of the capsule.
Since the fibres for the face occupy, as we have seen, the
junction of the two parts of the capsule, an isolated facial
palsy may result from a very small lesion in this situation ;
more frequently the adjacent fibres for the arm are involved
also. Tlie leg-fibres, l3dng behind the others, may escape in
a very small lesion paralysing face and arm, while damage
to the hinder part of the posterior limb causes a preponderant
paralysis of the leg. If the disease involves the hinder third
of the posterior limb, occupied by the sensory path, hemi-
ansesthesia is produced — loss of sensation on the opposite side,
head, trunk, and limbs, extending up to the middle line. The
loss is sometimes complete ; more often a touch is imfelt, while
a strong painful impression is perceived. The special senses
are also often involved — taste, hearing, and perhaps smell being
lost on the ansesthetic side, while vision to that side is lost in
each eye (hemiopia). The last may r^ult either from disease of
the external corpus geniculaf uui, or from damage to the fibres
from the tract to the oortex, or from damage to tlie optic thula-

LOCAL DIAGNOSIS. 175

mus, or from the latter to the cortex. Considerable damage to
one part of the capsule is often attended by slighter and transient
damage to the other part ; hence, hemiansesthesia may occur
at the onset of hemiplegia and pass away, and, conversely,
hemiansesthesia is often accompanied by transient weakness
of the limbs on the anaesthetic side. Convulsions rarely result
from disease in this region. Incomplete hemiplegia is, how-
ever, often accompanied by mobile spasm (athetosis, post-
hemiplegic chorea), but we do not know whether this is to
be ascribed to the disease of the capsule, or to that of the
adjacent ganglia, especially of the optic thalamus.

•

The corpora quadngemina are so rarely damaged alone,
that there is much uncertainty as to the symptoms that de-
pend upon their disease. The balance of evidence is strongly
against the old opinion that sight is impaired. The chief
effect is probably derangement of the internal and external
ocular muscles, sometimes impairment of certain ocular move-
ments, especially of the upward movement of the eyes and
elevation of the lids. An inco-ordination of movement, noted
in some cases of tumour, is probably the result of pressure on
the adjacent middle lobe of the cerebellum.

Damage to the cn(s cerebri causes paralysis of the face and
limbs on the opposite side, similar in character to that which
results from disease of the internal capsule, but accompanied
by palsy of the third nerve on the side of the lesion, and
therefore on that opposite the hemiplegia. Hemiansesthesia
may accompany the motor palsy, from implication of the
sensory path in the tegmentum of the cms. Hemiopia may
result from damage to the optic tract, but is very rare, since
the lesion is usually situated close to the pons, (jfiddiness is
common, but is usually ocular, and due to the affection of the
third nerve.

These facts of localization are complex, and those that
remain are still more so. It may be well, therefore, to post-
pone theii consideration until our next meeting.

LECTUEE XIV.

DIAGNOSIS OF THE SEAT OF DISEASE [Cirntinued): PONS,

. MEDULLA, CEREBELLUM ; BASE ; VENTRICLES— REVIEW OF

SYMPTOMS IN RELATION TO LOCALITY— BASAL LESIONS.

Gentlemen, — ^In the last lecture, you will remember, we
passed in review the symptoms that are produced by disease in
various parts of the cerebral hemispheres, in the cms cerebri,
and in the corpora quadrigemina. To-day we resume our
survey, and must notice first the effect of lesions in the mes-
encephalon, where the paths from the hemisphere to the limbs
are brought into proximity, where the chief cranial nerves
have their origin, and where an important junction is effected
between the fibres of the cerebellimi and those of the cerebral
hemisphere.

In the pons Varolii a lesion usually causes very character-
istic symptoms, due to the implication of the motor path and
of the cranial nerves that arise from the pons. Tumours that
grow slowly, however, and especially infiltrating timiours, may
attain a considerable size without causing characteristic symp-
toms. These symptoms maybe either unilateral or bilateral,
according as the disease affects only one or both sides of
the pons. Motor palsy is very common. Hemiplegia results
from one-sided disease, the limbs being, of course, paralysed
on the side opposite to the lesion. In the upper half of the

LOCAL DLAlGNOSIS. 177

pons, the upward facial path having crossed, the face may
suffer with the limbs exactly as in disease of the internal
capsule; but the chief characteristic of pontine hemiplegia
is the affection of the fifth, facial, or sixth nerves on the side
of the lesion, that is, opposite to the Hmbs, constituting the
"alternate hemiplegia" already described (seep. 58). The
tongue suffers as in ordinary hemiplegia. The palsy of
the fifth may involve motor or sensory parts, or both ; in the
latter case there is usually much pain, referred to the face,
and due to irritation of the nex^e-fibrea. When there i^
crossed palsy of the face, this is usually unaffected on the side
of the limb-palsy, but extensive 'disease may affect both sides
of the face. Paralysis of the sixth may be associated with
weakness of the opposite internal rectus, causing a paralytic
inability to move the eyes towards the side of the lesion ; they
are thus in conjugate deviation towards the paralysed limbs,
a direction opposite to that usually caused by disease of
the hemisphere. In bilateral disease, various combinations
of paralysis of limbs and the cranial nerves may occur. In
acute lesions of the upper part of the^ pons, the pupils are
often strongly contracted from irritation of the nuclei of the
third nerve, and, if these nuclei are invaded and destroyed,
the contraction gives place to dilatation and immobility.
Difficulty in swallowing and articulation result from
interference with the adjacent medulla. Convulsions are
rare, except in acute lesions, and are then sometimes
peculiar, affecting both arms or both legs. Tonic spasm
in the paralysed limbs is a common and often very-
marked symptom. Ehythmical movements are rare. Anaes-
thesia is less common than motor palsy, and the two are
often disproportioned. The explanation of this lies in the
fact that the motor path is in the anterior part of the pons,
the sensory in the outer part of the posterior portion, the two
being separated by the deeper transverse fibres. Tingling
and formication in the limbs are occasionally marked. Deaf-
ness is rare. Vision is never directly impaired. Taste may
be affected. Giddiness is sometimes severe. Respiration may
be irregular and abnormal in acute lesions, and the action

LECTURE mv.

of the heart irregular. Hyperpyrexia may result from aeute
leeiona, even from hEemorrliage, which elsewhere, at firat, de-
presses the temperature. Payehioal disturtanee is much more
frequent than might he expected, and is perhaps produced by
the damage to the fibres and grey matter which, as we have
seen, connect the cerebellum with the frontal and temporo-
occipital regions of the brain. It varies much in character.
The most vulnerable part of the medulla oblongata is the
region occupied by the nerve-nuclei at and below the apex
of the fotirth ventricle ; and the most characteristic symptoms
are those resulting from the damage to these nuclei. It is
rare for an acute lesion to cause symptoms in the limbs,
because a small lesion rarely oooupies the pyramidal region,
and any other than a very small lesion usually causes rapid
death by interference with the cardiac and respiratory centres.
Hence, also, if limb-symptoms do occur, they are slight;
they may be unilateral or bilateral. A small tumour may,
however, paralyse the limbs on one side, and the hypoglossal
nerve on the other ; but these symptoms depend more fre-
quently on disease outside the medulla, compressing it and
the nerve-trunks. The spinal accessory and glosso-pharyngeal
nerves may then suffer with the hypoglossal, causing the
group of symptoms that I have already described (p. 104).
Of acute lesions, hBemorrhage usually kills vdiii great
rapidity. Necrotic softening, from disease of the vertebral,
occluding its branches, sometimes causes symptoms of
sudden onset in the muscles supplied by the bulbar
nuclei. There is palsy of the lips, tongue, palato, pharynx,
and sometimes of the larynx, constituting acute labio-glossal
paralysis, or acute bulbar paralysis. The loss of power is
usually equal in the musdes of both sides, the lesion being
seated commonly near the middle line, The palsy is oeca-
sioually irregular in distribution. The onset may be attended
by subjective sensations in the legs, tingling, formication, ete,,
and rarely by some motor weakness. Chronic degeneration
of the nuclei causes a palsy of similar distribution, but differ-
ing iu its course, being gradual in onset and progressive in
course, and often associated with muscular atropky elsewhere.

LOCAL DIAGNOSIS. 179

Active disease of the middle peduncle of the cerebellum
causes very peculiar symptoms, the chief being an involun-
tary "forced" movement of the trunk on its longitudinal
axis, sometimes towards, sometimes from the side of the
lesion. It may amount only to an irresistible tendency to lie
on one side. There is usuaUy vertigo, and sometimes it is very
intense. The eyes may be directed to one side even when
there is no tendency to fall, or there may be a difference in
their height, or nystagmus. These symptoms are absent in
stationary lesions, and so probably depend on active irritation,
and not on a loss of nerve-structures. Associated with these
there are often other symptoms of disease of one side of the
pons — ^paralysis of the fifth nerve and of the opposite limbs.

The middle lobe of the cerebellum seems to be con-
cemed in some way with the maintenance of equihbrium,
and its disease causes imsteadiness in standing and walking.
The feet are placed wide apart, and the defective balance
may cause the patient to progress in a zig-zag manner.
Sometimes there is a tendency to fall forwards or back-
wards. The gait resembles that of a drunken man. There
is not the irregular movement of the legs common in loco-
motor ataxy. A sense of giddiness often accompanies the
unsteadiness, but is not its cause, since either may exist
alone. The imsteadiness may be present when the lesion
is stationary, as well as in active disease. Yomiting is also
frequent, but occurs only when the morbid process is active.
The intimate connection of the vagus with the nerve-struc-
tures concerned in equilibration is seen in the vomiting
that attends severe vertigo, such as that from ear disease,
and in the curious phenomena of sea-sickness, which pro-
bably depend on oscillations of the endolymph in the semi-
circular canals. This connection probably underlies the
vomiting from cerebellar disease. The vomiting may occur
apart from giddiness. The same combination of vomiting
and giddiness occurs in labyrinthine vertigo, but the giddi-
ness is more distinctly paroxysmal, and the vomiting occurs
only in connection with the giddiness. Disease of the hernia

n2

LECTURE XIV.

Spheres of the cerebellum, away from the middle peduncle,
causes per se no definite symptoms of diagnostic significance.
As NotLnagel first pointed out, the unsteadiness of move-
ment does not result from disease in the hemisphere imless it
is of Buoh a character as to compress the middle lobe, nnd it
is on this compression that the symptom depends. Compress-
ing lesions, such as a tumour, in either the middle lobe or
hemisphere, exert pressure on the pons, the tentorium limit-
ing the pressure to the subtentorial region. Hence there
is often slight weakness of the limbs, with signs of descend-
ing degeneration, increased myotatic irritability, etc., and
sometimes feelings of numbness and tingling, rarely anass-
thesia. When the tumour is in the middle lobe of the eere-
bellmn, the limbs 8u£er on both sides; when in one hemi-
sphere, the limbs suffer ohiefly on the opposite side. The
cranial nerves arising from the pons are also sometimes
compressed, and the sixth nerves suffer earlier and more than
others, on account of their exposed course over the convex
surface of the pons. The facial and auditory nerves some-
times suffer from lateral pressure. Convulsions are rare in
disease of the cerebeUmn, but tenic spasm, tetanoid in cha-
racter, may occur in tumours, and is probably due to
( on the pons

In the ventricles of the bram only two lesions are common,
hemorrhage and liquid effusions, and the localizing symptoms
are subordinate to those special to the morbid process.

It may be well to recapitulate the chief foots that we
have considered, looking at them from the side of the
symptoms instead of localities.

Persistent hemiplegia of the ordinary type may be due
to disease of the motor path anywhere above the middle
of the pons, or to disease of the motor cortex; but transient
hemiplegia only shows that the disease is near the motor
path or centres, so that it can affect them indirectly. Since
the most common seat of disease causing hemiplegia is the

corpus striatum and internal capsule, there is always a pre-
sumption that simple hemiplegia is due to a lesion in this
situation. If the faee and tongue escape, the disease may
be anywhere in the path between the medulla and cortex,
hut there is a presumption that it is above the intemaJ
capsule, where the elements of the motor path are wider
apart., and partial escape is more probable. The same is true,
a fortiori, of partial hemiplegia affecting face and tongue,
or face and arm. These, if of sudden onset, axe moat
frequently due to disease of the cortex, sometimes to thai
of the white substance, very rarely to a lower l^on. I say
" if of sudden onset," because when a chronic lesion involves
the motor path anywhere, the gradual impairment may be
at first partial in extent ; but if the path, at the seat of
disease, occupies a small area, all parts soon sufier, and the
initial weakness of one limb, as it deepens in degree, soon
extends to the other parts of that side. Considerable loss of
sensibihty on the extremities of the limbs, not through the
whole side, probably indicates a lesion of the cortex or white
substance beneath. Well-marked hemiansesthesia with hemi-
plegia indicates an extensive lesion of the posterior limb of the
internal capsule; and conjoined hemiopia indicates that the
lesion is extensive at the posterior part of the capsule, and has
damaged the optic path, probably at the corpus genieulatum,
or optic thalamus. Affection of the other special senses has
the same indication of extensive mischief in this situation, but
it is more common to have these symptoms without than
with persistent hemiplegia, because a lesion in this region does
not often destroy the motor part of the capsule. Paralysis of a
cranial nerve on the side opposite to the hemiplegia indicates
a lesion at the level of origin of that cranial nerve — ^the cms
in the case of the third nerve, the middle of the pons iu that
of the fifth, the lower third of the pons in the case of the
facial or sixth, the junction of the pons and medulla in the
case of the auditory, the medulla lq the case of the hypoglossal
or spinal accessory. It must be remembered, however, that
the localizing significance of these associations depends, in the
case of acute lesions, on their simultaneous onset.

4

LECTURE XIV,

Ptosis, slight in degree, on the side of the hemiplegia, indi-
cates that the lesion is in or near the cortex, with a slight
probability that it involves the parietal lobe, or subjacent
white substance. Coujtigate deviation of the eyes from the
side paralysed, or towards it if there are convulsions or much
rigidity of limb, ia of no localizing significance; towards the
side paralysed, without any indications of spasm, it suggests,
but does not prove, an affection of the pons; if there is
complete loss of power of the external rectus, and slighter
loss of power of the opposite internal rectus, the lesion is
certainly in the pons. General convulsions are of no
localizing significance : those that begin locally, if they
ooeur at the onset of an acut« lesion, suggest, and, if they
attend a chronic lesion, practically prove, that the disease
is in, or just below, the cortex.

Paralysis of the cranial nerves has a far more definite
significance when several nerves are affected, than when one
suffers alone. The possible seats of the disease are numerous
in the latter case, while in the former they are few, and often
there is only one position in which a single lesion can cause
the combined effect. We may glance at a few of the more
important indications. Palsy of one hypoglossal is probably
due to disease outside the medulla, and this is certain if the
palate and vocal cord (spinal accessory) are affected also. Para-
lysis of both sides of the tongue is usually due to disease of the
nuclei (very rarely to symmetrical disease of the cortex), and
the lips usually suffer with the tongue. If the face is paralysed,
we must note first whether the lower part suffers chiefly, and
the muscles of the forehead and eyebrow escape, and electrical
excitability is normal, or whether aU parts are involved, and
faradaic irritability is lost. In the first case the lesion is above
the nucleus, and is probably above the internal capsule. In
the second it may be in the nucleus, the fibres of origin in
the pons, at the base of the brain, or in the temporal bone.
Paralysis of the lower part of the face and tongue on one
side indicates disease of the hemisphere, and probably of the
cortex. If the auditory nerve suffers with all parts of the
facial, and there is no ear disease, the lesion is at the base.

[

ParaljeiB of all parte of ths face on each sida is due to
symmetrical disease of the facial nuclei, or of the nerve-tnmka
at the baae.

Paralysis of one ooular nerve ia usually due to disease
at the base ; that of all the uerves of one eye indicates
disease about the orbital fissure ; that of all the nerves of both
eyes, degeneration of the nuclei. Paralysis of the sixth and
facial (without the auditory) is due to disease within the pons.
Paralysis of the sixth and fifth indicates disease outside the
pons ; although the nerves aiise at some distance from each
other, the sixth nerve, as it enters the dura mater, is nearer
the fifth than ia any other nerve.

The diagnosis of the seat of disease at the base of the brain
has to be made chiefly in the ease of chronic and subacute
lesions, especially tumour and meningitis. In haemorrhage
the local symptoms are rarely prominent — they are lost in
the more diffuse symptoms that attend severe haemorrhage.
In all basal disease the characteristic symptoms ore due to
the interference with the cranial nerves. In disease of the
posterior fossa, the fifth and those below are Uable to suffer,
and with them the motor tract, causing weakness in the limbs,
usually hemiplegie in character. The distinction from disease
within the pons depends on the circumstances that the nerves
more often suffer before the motor tract to the limbs when
the lesion is at the base, and that the combination of nerves
affected is different. Thus, at the base, the fifth and sixth
nerves may suffer together, the facial and auditory, the spinal
accessory and hj-poglossal. The nerves are often irritated before
they are [loralysed, and such irritation of the fifth nerve often
causes very severe and persistent neuralgic pains in the region
Bupphed by it, and sometimes (although rarely) trophic
changes in the eyeball. Rigidity in the limbs may occur from
the some cause, espeoiaily when the anterior pyramids of the
medulla ore exposed. General convulsions are rather more
common from disease outside, than from that within the pons.
Pressure on the middle peduncle of the cerebellum may give
rise to intense vertigo and forced movements.

In the middle fossa, symptoms are chiefly produced by

184 LECTURE XIV.

tumours, and the most important are symptoms of irritation
and paralysis of the fifth nerve. The Q-asserian gangKon is
often involved, and trophic changes in the eyeball are com-
mon. In the interpeduncular space, morbid processes affect
one or both third nerves, and often also one or both motor
tracts in the cms. Less commonly one optic tract is involved,
causing hemiopia. Convulsions are rare.

In the anterior fossa, properly speaking, only the olfactory
nerves suffer, but disease usually involves also the neighbour-
hood of the sella Turcica, and damages one or both optic
nerves, and the nerves to the eyeball in the wall of the
cavernous sinus or at the orbital fissure. Occasionally the
optic chiasma is involved; the fibres that decussate suffer
chiefly, causing temporal hemiopia.

LECTUEE XV.

DIAGNOSIS OF THE NATURE OF THE LESION— PATHOLOGICAL

FACTS BEARING ON DIAGNOSIS.

GrENTLEMEN, — ^We pass now to the last diagnostic problem
that we have to consider, that which is, beyond all question,
the most important — ^the nature of the disease. The diagnosis
of the seat of the lesion is a problem of fascinating interest to
the physician, but the limits of its importance to the patient
are quickly reached. It is important to the latter chiefly as
affording, in some instances, a guide to prognosis. But on
the nature of the lesion depend not only the prognosis for the
most part, but the treatment altogether. This pathological
diagnosis is, as a general problem, far more diflScult than the
anatomical diagnosis. It is true, the nature of the disease
can sometimes be determined with ease and confidence ; more
often, however, it is a question of much difficulty and some
imcertainty.

We may ask, in the first place, what are the morbid pro-
cesses that we have to deal with ? We may leave out of the
question fliose that are of extreme rarity, and consider only
those that you are likely, at some time or other, to meet with
— ^that constitute about ninety-nine out of every hundred
cases of organic brain-disease that come under observation.

186 LECTURE XV.

They are not very numerous, fortunately for ub. They arc
inflammation, chiefly of the membranes, hemorrhage, necrotic
softening, tumours, aneurism, abscess. Congestion and
anaemia of the brain, which are not, properly speaking,
organic diseases, we shall have to notice incidentally, and
likewise three degenerative diseases — the bulbar degenera-
tion that I have already mentioned to you, termed, from
its symptoms, " labio-glosso-Iaryngeal paralysis " ; " general
paralysis of the insane," which differs from other varieties of
insanity in the obtrusive physical symptoms that form part
of its manifestations, and often come into diagnostic relation
to other diseases ; and, lastly, " disseminated " or " insular
sclerosis."

To understand many of the indications ol these lesions,
it is needful for you to know certain facts regarding their
mode of production and pathology. It is impossible for
me to enter, however briefly, into the pathology of all these
lesions. But the diagnostic indications, that I shall have to
describe to you, will be clearer if some facts, regarding espe-
cially the acute lesions, are fresh in your minds. It may be
well, therefore, for me to depart, in this lecture, from the
special subject of this course, in order to direct your attention
tfl these points.

Although we shall deal with congestion of the brain only
incidentally, you should know that doubt has been thrown on
the very occurrence of this condition — doubt that is a reaction
from another extreme. The state of the blood-vessels of the
brain after death is very little indication of what their condi-
tion has been during life. Before this fact was known, post-
mortem distension was regarded as evidence of ante-mortem
congestion, and an extensive symptomatology was elaborated
on insufficient grounds, — a symptomatology that has, to some
extent, survived its data. Further, "congestion of the brain,"
like " congestion of the hver," is a ready diagnostic refuge,
seductive in its simphcity, and pleasing in its precisenesa;
easily affirmed, and not easily disproved. On this basis of
pure diagnoatio fancy, as I hinted in a previous leoturd, a

DIAGNOSTIC PATHOLOGY, 187

Bymptomatology has also grown up, and even statistics have
been omasBed, the value of wliich is considerably telow zero.
It is not surprising tliat from such reasoning a reaction has
arisen, and the influence of cerebral congestion in causing
symptoms has been narrowed almost to the vanishing point.
Even its pathological possibility has been denied, on an o!d
ground that the total amount o£ blood within the eranio-
vertebral cavity cannot vary because the cavity is a closed
one. The truth probably lies between the two extremes.
Cases in which the pronounced symptoms can reasonably
be ascribed to active cerebral congestion are rare — far less
frequent than might be imagined from the place that the
rendition still occupies in the written and unwritten
pathology of the present day. But the state probably
does occur, and does cause symptoms. The mobility of
the cerebro-spinal fluid permits the condition of the vessels
to alter in various parts of the brain. If the cranio-vertflbral
cavity were hermetically closed, the variations could, perhaps,
be only relative, not absolute. But the numerous foramina
of this cavity are occupied by structures of bftle resistance,
which may yield in some degree. Moreover, the large surface-
veins of the spinal cord, and still more the enormous plexuses
outside the spinal dura-mater, must constitute an important
means of adaptation. The processes of secretion and absorp-
tion of the cerebro-spinal fluid, always in constant operation,
must be influenced by the degree of pressure, and may quickly
vary with it. The enormous variations in the amount of
blood in the nerve-centres after death may be admitted as
afEording some evidence that variations are possible during
life. Lastly, the eye is closed at least as completely as the
oranio-vertebral cavity, and variations in the amount of
blood within it may be aetually seen. If, then, you should
hear the possibility of cerebral congestion denied, remember
that the grounds on which it is denied are not themselves
unimpeachable .

Cerebral hsemorrhage is almost always due to the rupture
of an artery, very rarely to that of a vein. Veins rupture

LECTUKE X\\

cliiefly under Biich extreme pressure as, for instance, attends
strangulation, and, iinder the same circumstanees, capillaries
may give way and cause minute extravasations. Arteries,
however, rapture only when their walls are diseased, and they
may then give way without any extraordinary pressure of
the blood. Before they hurst, their wall yields before the
hlood-pressure ; becoming extended, it becomes thinned. This
hidging of the wall constitutes an aneui-ism, and hence it is
that the hemorrhage always results from the rupture of an
aneurism. A healthy wall never yields before the hlood-
preesure ; local change, lessening the elasticity of the wall,
always precedes dilatation. The aneurisms that result may be
on the large arteries of the base or surface, and are then of
some size ; or they may be on the small arterial branches,
especially on those that go to the central ganglia, and are then
minute. They are often called "miliary aneurisms," from
their small size. The larger aneurisms on the arterial trunks
are meant when we speak of " intracranial aneurism," without
the qualification of "miliary," They are often single, and
always few. The miliary aneurisms are always numerous ;
sometimes there are hundreds scattered through the brain.
The difference in name has its justification, not only in the
difference in size, but also in the fact that the miliary aneur-
isms cause no symptoms until they rupture, while the larger
aneurisms sometimes cause considerable disturbance, especially
when they are seated on a vessel at the base of the brain.
The local change in the wall that permits the vessel to yield
before the pressure of the blood is usually syphihtic disease or
inflammation of the wall — either traumatic inflammation, or
more often that which results from imperfect obstruction by a
plug that comes from an inflamed cardiac valve, and excites an
inflammation in the wall of the vessel similar to that in its
source. The aneurism sometimes results from simple fibroid
degeneration, but rarely from the fatty degeneration that is
termed atheroma. The miliary aneurisms are chiefly the effect
of a primary degeneration of the wall, of which an important
cause is the strain to which they are exposed, aided by the
degenerative tendency that is incidental to age, and that

DIAGNOSTIC PATHOLOGY. 189

attends certain constitutional diseases, especially kidney disease.
Thus the agent in their rupture, the blood-pressure, is in some
measure the agent of their production. The reason why they
are so frequent on the branches to the central ganglia is probably
because these small arteries come off directly from a large
vessel, and so the blood-pressure within them is higher than it is
in most arteries of the same size. Although the degeneration
differs in nature from the atheroma on the larger arteries of the
base, their causes are in part the same, and therefore the two
often coincide. Indeed, it has been suggested by Nothnagel
that the atheroma may aid the production of the minute
aneurisms, by the loss of elasticity in the larger arteries that
it involves ; this renders the pulse-wave more sudden in the
branches. From these facts it follows that, while there is
no necessary relation between the two, atheroma is present
in three-fourths of the cases in which there are miliary
aneurisms (Charcot and Bouchard). It is important to
remember this fact. Certain general diseases cause a tendency
to haemorrhage, apparently from an acute degeneration of the
walls of the smaller arteries. These are scurvy, purpura,
pernicious ansemia, and especially leucocythaemia. They may
cause cerebral haemorrhage. The actual rupture of an artery
may be produced by the strain of some muscular effort, or it
may occur when the patient is at perfect rest, even, indeed
often, during sleep. The frequency of rupture during sleep is
remarkable. Perhaps it is determined by the influence of
gravitation ; or rather by the loss, in the recumbent posture,
of this aid to the return of blood from the head. Possibly,
moreover, the contraction of the vessels, that is said to attend
sleep, is of arteries smaller than those that are the seat of
miliary aneurisms, and may even increase the blood-pressure
in the latter, and help to determine rupture.

The most frequent seat of haemorrhage is the corpus
striatum, the vessels that rupture being especially the
branches of the middle cerebral that pass through the len-
ticular nucleus to the caudate nucleus, or optic thalamus.
The extravasation ploughs up the adjacent parts, and usually
tears through the internal capsule, causing hemiplegia. Often

LECTURE XV,

it extends info the wliite aubstanee of the hemisphere, or
buTBts into the lateral ventricle. Although hcemorrhagea
may occur in any part of the brain, they axe comparatively
rare in the cortex — a fact of considerable diagnostic import-
ance. Meningeal hsemorrhage tisually results from the
rupture of an internal extravaeation, or from traumatic
causes, but it sometuneB occurs in maladies that entail a
hfemorrhagie tendency, and in the course of severe acute
specific diseases. Ventricular htemorrhage is also usually
secondary, rarely primary.

The extravasation of blood destroys the tissue-elements
by lacerating them, and it compresses the adjacent structures.
All mechanical injury irritates nerve-elements at the moment
of its occurrence, and the irritation that attends hsemorrhage
is probably one agent in the production of the loss of con-
sciousness that usually attends the onset. This is doubtless
due also to the pressure to which the whole brain is exposed,
striking evidence of which is afforded by the extent to which
the falx is sometimes bulged to the other side. It is to this
compression that the "indirect" symptoms are chiefly due.
But the adjacent damage thus produced is not usually intense
iu degree, although it is wide in range, and the ultimate
recovery from these indirect symptoms is often perfect.

The term " softening of the brain " is used in medicine
in its literal sense, Tou have probably already discovered
that the popular use of the word is somewhat metaphorical,
and that it is applied to various conditions in which there
is a slow failure of mental power — conditions which we call
by other names, because there is no actual softening. The
chief pathological causes of softening are inflammation and
arrest of blood-supply. There is, indeed, a third form,
simple chronic softening, but it is excessively rare (not more
than haH a dozen well- authenticated cases are on record),
and we need not, therefore, concern ourselves with it. In-
flammatory softening we may also leave for the present ; it
is rare, except as the result of injury (which is beyond our
province) , or as the first stage of abscess, and that we shall

DIAGNOSTIC PATHOLOGY. 191

consider separately. The arrest of blood-supply is due to
the obstruction of an artery, and causes a sudden cessation
of all the processes of nutrition that maintaui the vitality of
the tissue-elements. It is, therefore, often called "necrotic
softening." This arrest of blood-supply, whatever be its
cduse, always involves derangement of the collateral circu-
lation, and considerable secondary inflammation about the
necrosed area. Hence the extent of the damage that falls
short of destruction is usually relatively greater than in
haemorrhage.

Two pathological processes may cause the occlusion of an
artery. A plug, from some distant source, may be carried
into the vessel by the blood, and be arrested where the artery
is narrower than the plug — "embolism" — or the clot may
be formed in the artery by coagulation of the blood at the
spot obstructed — "thrombosis." Embolism is the result of
a morbid process elsewhere in the vascular system, commonly
in the heart. Thrombosis is the result of a local disease of
the artery, by which its calibre is narrowed and its inner
surface is changed. The alteration in the wall of the vessel
is usually the result of atheroma or of syphilitic disease.
The process of occlusion is often aided by a change in the
blood, rendering it more prone to coagulate, or by a slower
movement of the blood, giving it more time to coagulate.
These may not only aid arterial disease in causing the
occlusion, but may also sometimes cause thrombosis when
there is no change in the wall of the vessel.

Although the processes of thrombosis and embolism are
thus distinct, and usually occur under different conditions,
the two may be combined in a secondary manner, which
does not, however, affect the important and essential distinc-
tion between them. If an artery is obstructed by embolism,
the distal portion may be further occluded by coagulation of
the stagnant blood. Again, if a clot forms in an artery, it
may be detached, and may be moved a little further on. This
is, de facto, embolism, although the result of thrombosis, and
classed as thrombosis since the clot is formed in the artery
occluded, although not at the point of occlusion. Again —

192

LECTURE XV.

and tliis is very important,— under certain circiimBtances 1
influences that cause thromtosis may also cause embolism. A
state of the blood, inclining it to coagulate, may cause a clot
to form, not in an artery, but in the heart, especially when
there is valvular disease, and the clot may be detached. We
shall presently see the importance of this consideration.

In emboham the source of the plug is between the pul-
monary capQlaries and the artery ohstnicted, and it usually
comes from the left side of the heart, from a diseased valve,
or from a clot in one of the cavities of the heart (especially
from the auricular appendix), rarely from the aorta or the
lungs. The valvular disease that is most frequently the
source of a plug is mitral constriction, perhaps because the
alow flow during the diastole favours the collection of eor-
puflcular vegetations on the valve, and the rapid flow
during the systole of the auricle favours their detachment.
When the endocarditis is septic, and the vegetations contain
organisms, the obstructing plug is apt to excite similar in-
flammation in the brain ; and if the endocarditis is virulently
septic, or the plug comes from a septic focus in the lungs,
the inflammation in the brain may go on to suppuration.

The arterial disease that causes thrombosis is chiefly, as
I have said, atheroma or syphihtio disease. The latter
occurs at all ages at which acquired syphilis is prevalent ;
it is rare from the inherited disease. The atheroma is
essentially a senile change, but its oecurrenee is facihtated
and hastened by Bright's disease, and some other influences.
It increases in frequency as life advances. Both atheroma
and syphilitic disease of the arteries are sometimes sym-
metrical, and may thus give rise to symmetrical lesions in
the brain, and symmetrical symptoms in the hmhs. Re-
member that traumatic injury, such as a fall on the head,
or a blow, may cause arterial disease, which may lead to
thrombosis long after the injury, perhaps after it has been
long forgotten.

Thrombosis may occur, not only in the arteries of the
brain, but also in the cerebral siauses and veme.

reme. That in J

DIAGNOSTIC PATHOLOGY. 193

the sinuses is an extremely grave affection, not only by reason
of its effects, but also because it is generally due to disease
that is in itielf most grave, and of which the thrombosis
forms only a terminal incident. Its causes are of two kinds.
The first is general disease, favouring clotting by changing
the quality and retarding the flow of the blood. This form
occurs with especial frequency in young children, and oc-
casionally in very old age. Now and then it occurs at the
end of phthisis, after childbirth, or in the course of cancer.
In the young, its most common cause is exhausting diarrhoea,
or some other prostrating disease, such as an acute specific.
The sinus affected in these cases is almost always the superior
longitudinal. I drew your attention, in an early lecture
(p. 41), to the conditions of the circulation in the veins and
sinuses, that render a general cause so effective. The second
great cause of thrombosis in the sinuses is adjacent disease.
Almost any sinus may be thus affected. The disease is often
in the bones of the ear or of the skull ; sometimes it is out-
side the skull, as erysipelas of the scalp. This form occurs
with nearly equal frequency throughout life, but it is rare
at those periods at which the primary thrombosis is most
frequent — infancy, and extreme old age. Inflammation of
the wall of the vessel usually precedes coagidation of the
blood within it. You may remember that I drew your
attention (p. 43) to the communications between the sinuses
and the veins of bones and exterior of the skuU, which
permit the ready extension of morbid processes.

The clot that forms in a sinus often extends into the veins.
The obstruction of a vein causes intense hypersemia of the
part from which the blood should be removed by the vein ;
the capillaries rupture, and the minute extravasations that
result may occupy almost all the area of the affected region.
Some softening results, but there is not the wholesale soften-
ing that is produced by arterial occlusion.

In text-books on Medicine you will find very little about
thrombosis in the cerebral veins, as distinguished from
that in the sinuses. The condition is rarely seen post-
mortem, but it is now and then met with. I believe,

o

194 LECTURE XV.

however, that it is both a frequent and an important lesion,
and I must digress for a few minutes to give you the
grounds for my "belief. The condition is rarely seen in the
post-mortem room, because, if a patient dies, the clot ex-
tends into the sinus, and the case is regarded as one of
thrombosis in a sinus. Thrombosis, limited to a vein,
although it may be aerious in its effect on the brain, is
not a lesion that inyolTes much danger to life. The patients
recover, nnd we can only infer the occurrence of the lesion
from the character of the symptoms. I have seeu it post-
mortem in phthisis, and it has been observed iu other
conditions of prostration. It is occasionally met with in the
course of tubercular meningitis, and may, I believe, occur
■when there is meningeal tubercle, but no iuflamraation.
When it has been met with as an isolated lesion, one or two
large veins over one hemisphere have been found occluded.
The symptomB that suggest its occurrence are most frequently
met with in children who are suffering from debility, ex-
hausting diseases, especially acute specific diseases, or after
blows on the head. Now and then they occur in very
yoimg children without any exciting cause; and I have
obser\'ed that such cases, like infantile spinal paralysis,
frequently occur during the hot season of the year.

The symptoms are these r — ^young children are attacked
with hemiplegia, and recover, usually with some persistent
weakness in the arm, often with mobile spasm in the limbs, —
" infantile hemiplegia," or " infantile spastic hemiplegia,"
the cases ore termed. The onset is often attended with
severe convulsions, and convulsions may recur, even through
life, affecting chiefly the paralysed limbs, and constituting
a distinct variety of epilepsy.* We have already seen, in
the lecture on the local diagnosis, that such symptoms
indicate a cortical lesion. The conditions under which this
hemiplegia comes on make it almost certain that the lesion
is thrombosis. Thrombosis in arteries is a very rare post-
mortem lesion in childhood, far more rare than is combined

DIAGNOSTIC PATHOLOGY. 195

thrombosis in sinuses and veins. The initial symptoms in
these cases resemble closely those that have been observed
in the rare cases in which a vein of the cortex is occluded
in an adult. When children die with such symptoms as
I have mentioned, we commonly find thrombosis in the
longitudinal sinus, and veins opening into it. As I have
said, the thrombosis probably extends into the sinus, and into
the veins of the other hemisphere, during the final period.
Prom these considerations it seems to me practically certain
that, in the cases that do not die, there is thrombosis in one
of the surface veins that ascend to the longitudinal sinus,
in which, for the reasons I gave you, the circulation is so
slow, and the conditions are so favourable to coagulation.
When such cases die in later life, the appearances are in
perfect harmony with this view. We do not find any
cavity, such as we do find when an artery has been
occluded by embolism in childhood, and the subject dies
in adult life. We see that in a certain area of the cortex
the convolutions are shrunken and indurated — exactly the
state that we should expect from the appearances presented by
recent cases, and very unlike that observed in cases in which
we are sure that there has been occlusion of an artery.

These cases are not at all infrequent. They constitute
the majority of cases of sudden cerebral disease in child-
hood. The hemiplegia may be transient, when the lesion
is near, but not in, the motor part of the cortex; and
probably, in early infancy, the initial hemiplegia, if slight
in degree, may altogether escape observation. Most cases
of epilepsy dating from infancy, in which the fits are one-
sided, are of this character. We can very often trace slight
indications of hemiplegia, in trifling weakness, slight
shortening of the limbs, or in a slight degree of the mobile
spasm that is so marked in the more severe cases.

There is another frequent form of infantile cerebral
palsy about which you will also find little in your manuals.
In this form, paralysis of one side, or more commonly of
both sides, is what is called " congenital," that is, the child

o 2

Itrtf LECTURE XV.

comes into the world with it. The affection, like most
others of a congenital character, is popularly attributed to
" maternal impressions," to some emotional distm-hance that
the mother endured during her pregnancy. The designa-
tion is not altogether inapt, for the actual meehanism is a
maternal impression, although it is one ia which the
mother is the agent, and not the euhject. The cause is
the injuiy the child suffers during its passage into the
world. The affections are most common in first children,
and after lengthy labours, and they arc more common
when the presentation is unnatuj-al than when the head
presents. They occur in forceps cases also, but probably the
effect is due much less to the inatrument than to the con-
ditions that render instrumental aid necessary. The chief
pathological mechanism is meningeal hieraorrhage, compress-
ing certain parts of the brain. In children who die, there is
usually a thick layer of blood over part of the cortex. The
clot often lies over the motor convolutions, and may extend
from the longitudinal fissure to the fissure of Sylvius.
There is sometimes extensive sub-tentorial hemorrhage from
laceration of the cereteUum, but the blood over the cerebrum
seems generally to come from the meningeal vessels, and not
from the brain-substance. The child often suffers from con-
vulsions during the first few days of life, and the limbs may
even then be observed to be motionless. After a time some
movement returns, and the ultimate condition is a combina-
tion of palsy and spasm, with spontaneous movements, and an
irregular choreoid inco-ordination, constituting what has been
variously termed " double spastic hemiplegia," or "bilateral
athetosis," or "congenital chorea." The irregular movements
are chiefly marked in the arms ; in the legs the spasm is chiefly
tonic, extensor, but with occasional flexion of the knees, espe-
cially on an attempt to walk, and often there is some contracture
of the calf-muscles. In many cases there is mental defect,
which may amount to actual idiocy. The children do not
begin to walk until late, often not until the age of six or
eight, and their walk is always peculiar. Adductor spasm in
the legs may cause a "cross-legged" progression. You may

DIAGNOSTIC PATHOLOGY. 197

sometimes recognize the unfortunate subjects of this defect in
the streets by their peculiar gait. In addition to these motor
limb-symptoms, there are often symptoms of paralysis of
the muscles of the neck. The children are imable to keep the
head up during the first two or three years of life. I have
observed this neck-palsy chiefly in cases of foot or breech
presentation. We do not know whether it is due to injury
to the bulbar nerves (as the spinal accessory), or to their
compression by extravasated blood, or to damage from the
inflammation excited by such extravasation. It is conceivable
that the anterior pyramids of the meduUa may be directly
injured, and that this may cause some of the limb-symp-
toms; but this is on the whole improbable, since haemorrhage
over the cerebrum and about the medulla may coincide. The
symptoms sometimes suggest that the inflammation about
the meduUa closes the openings into the fourth ventricle, and
that internal hydrocephalus may thus be produced. Occa-
sionally the legs are affected in much greater degree than the
arms, perhaps because the haemorrhage is situated over the
upper part of the motor convolutions (leg-centre), or these
may even be directly damaged when the edges of the sagittal
suture greatly overlap. Such cases have been termed " con-
genital spastic paraplegia." Again, the tongue and lips may
be weakened out of proportion to the other parts, and difficulty
in deglutition and in speaking may persist through life.
Some of you saw such a case a few days ago in my out-patient
room. This bidbar palsy may be the residt of damage to
the bulbar nerves, such as I have just mentioned, or it may
be due to symmetrical haemorrhage over the lower parts of
the motor convolutions, which may produce symptoms
closely resembling those that are caused by disease of the
medulla oblongata.*

Inflammation of the brain, except from injury, or in the
form of abscess, is so rare, that we may leave it out of con-

• The relation of these symptoms to injury during birth was pointed out by
Dr. Little in 1862. Some valuable facts relating to the question have been
recently published by an American lady, Dr. McNutt (** American Journal of
Medical Science." Januaiy, 1885).

Bideration. The chief form of intracranial inflammation is
that of the membranes — meningitis. Inflanimation of the
dura mater is rare, except from injury ; the variety of chief
medical importance is the inflammation of the pia mater, or
pia arachnoid, since both the softer membranes usually suffer
together.

Meningitis maybe simple, purulent, tubercular, or syphilitic.
It may affect chiefly the convexity, or chiefly the base, or
may be still more partial. Simple meningitis is rare except
from exposure to the sun, and then it is seated over the con-
vexity of the brain ; but it occurs in limited extent from local
disease of various kinds, such as tumour, or softening that
is situated near the surface. Purulent meningitis is due
generally t« suppuration elsewhere, either adjacent to the
membranes, as in caries of the bones of the skull, or disease
of the internal ear. Distant suppuration produces it chiefly
by the mechanism of pysemia. It may attend the septictemia
of the puerperal state. Occasionally it occurs in the course of
acute general diseases, and in children it may develops when
no condition can be discovered to which it can be secondary.
Purulent meningitis is often general, affecting both the base
and the convexity, and in children the spinal membranes also.

The most conamon form of meningeal inflammation is the
tubercular. It occurs in childhood with especial frequency,
generally in families in which there is some tubercular taint.
In adults it occurs chiefly in those who are actually suffering
from tubercular disease of the lungs, but in youths of both
sexes it may be primary. The membranes of the base are
usually affected far more than those over the convexity, and
the most characteristic symptoms of the disease are due to the
damage to the cranial nerves. Hemember that tubercle of the
membranes is not quite the some thing as tubercular menin-
gitis. Tubercle may exist without inflammation, and prob-
ably always precedes inflammation, which may be excited by
some influence that may seem to be the cause of the sjTUptoms.
If the membranes were previously healthy, the exciting
cause would be without effect. Massive tubercle, constituting
a tumour, may be attended with intercurrent tuberoular

IHAGXOSTIC 1

meningitis, and mixed, symptoms of a complex character
may result.

Syphilitic meniitgitia is almost always ehronic. It may
involve the membranes of the base, or of the convexity, but is
often partial in distribution. It consists of a combination of
inflammation and growth, and often extends about an actual
syphilitic tumour, irritating and damaging the adjacent
structures. Remember that the nerves are often damaged
by Byphihtic disease when there is no actual meningitis.
They may be affected by a syphilitic neuritiB, an inflamma-
tion of the sheath of the nerve ; or the sheath may be the
seat of a syphilitic growth. Such growths on the uerves
are sometimes sjTnraetrieal ; the same cranial nerve may
thus be paralysed on each side.

Almost any kind of tumour may occur in the brain, but
some, as fatty tumours, which are coromon elsewhere, are
extremely rare in the brain, while others, as ghoma, are
almost confined to the cerebral tissue. The most common
intracranial gro\vths are tubereidar and syphilitic; next
comes glioma, then sarcoma, and then cancer. Other forms
are rare. Tubercular tumours are most frequent during
the first twenty years of Ufe. Syphilitic growths occur
chiefly during the period of active adult life, from twenty-
five to fifty. The only iniflueuce that ever seems to eTcife.the
development of a tumour is injury; this more commonly
causes a tumour springing from the membranes than one
beginning in the brain-substance. Growths that spring
fi'om the dura mater usually compress the brain - tissue.
Those that spring from the pia mater, or develope within the
brain, may either compress or invade the cerebral substance.
The oharacteristic of ghoma is its invasive tendency. It
developes in the interstitial tissue of the brain, and encloses
and destroys the nen'e -elements. It enlarges the pai-t of
the brain iu which it occura, and there is no sharp hue of
demarcation between the tumour and the brain-substance.
On the other hand, most other tumours, and among them
tubercular, syphilitic, and sarcomatous growths, do not

invade the brain-tisaue, in the strict sense of the word ; it
perishes hefore them, partly by the compression they exert,
partly in oooaequence of the inflammatory irritation that
they produce, and which is shown by the zone of soffeniug
that usually surrounds them. In each ease, however, the
fuucfional impairment of the cerebral tissue does not always
correspond to the apparent structtu^l damage. The nerve-
fibres that are compressed before the growtli in the one case,
or are included in the growth in the other case, may retain
some functional power, and the symptoms of loss of function
may be much less than might he anticipated from the position
and the extent of the lesion. Again, the irritation that is
caused may be greater in degree, and wider in range, than
the size of the tumour would suggest. I mentioned this fact
to you on a former occasion, and remind you of it now on
account of its importance. Lastly, you should know that
one form of tumour, ghoma, is occasionally the seat of a
sudden hEeraoirhage.

Abscess of the brain is usually due to injury to the brain,
to adjacent suppuration, especially bone disease, or to suppura-
tion at a distance, especially in the lungs. Curiously, it is rare
in general pycemia. Ear disease is its most common cause.
It occasionally results from disease of the orbit or of the nose.
The abscess may be in any part of the brain. Caries of the
middle ear usually causes abscess in the temper o-aphenoidal
lobe, rarely in other adjacent lobes. In caries of the mastoid
cells the abscess is often in the cerebellum. The symptoms
produced are frequently slight in proportion to the size and
position of the abscess, and it is common for the disease to
run an almost latent course until acute symptoms arise.
These are often due to ruptiu-e, which may occur into the
ventricles, or into the membraues, and its sj-mptoms are oi
extreme gra^-ity, quickly fatal.

Did time permit, I might with advantage point out to you
many other facts of etiology and pathology that aid us in
our diagnostic effort. Some of them I may mention in the

DIAGNOSTIC PATHOLOGY. 201

description of the method of diagnosis to which we shall
pass in the next lecture. But there is one general law that
I must mention before I leave this part of the subject.

Whatever be the morbid process that causes damage to
the brain, the symptoms are due to the latter; and the
changes in the nerve-elements are much the same, whatever
be the nature of the morbid process that causes these
changes. We do not recognize this in our mode of speaking
of these diseases. We speak, for instance, of "syphilitic
disease of the brain," but the damage to the nerve-elements
is never syphilitic. The syphilitic disease is outside them,
sometimes altogether away from them, and it causes in
them simple processes of degeneration, etc., on which the
symptoms depend. This is not a mere theoretical refine-
ment; it is of great practical importance, especially in
regard to prognosis, and occasionally important in diagnosis.
We shall see that we sometimes look to the result of
treatment — ^to the effect of the administration of "anti-
syphiUtic'' drugs — to confirm our diagnosis. But such
treatment has no direct influence whatever, so far as is
known, upon the changes in the nerve-elements. We may
lessen or remove the syphilitic lesion that has produced the
changes in the nerve-structures, and then certain kinds of
damage will pass away, especially that which results from
pressure, as of a growth. Other kinds of damage cannot
pass away, as, for instance, necrotic softening, due to
syphilitic disease of the wall of the vessel. You may remove
this disease, but you cannot restore the brain-tissue that is
dead, and no more recovery is possible for it than in a
corresponding case of embolism. Symptoms may pass away
in each case, but only when they are " indirect " in nature ;
and " direct " symptoms are as lasting in one case as in the
other. Hence, before we can take the absence of improve-
ment under treatment as an indication that a disease is not
syphilitic, we must consider whether the change in the nerve-
elements is one from which recovery is possible when the
cause is removed. Speaking generally, the more quickly the
changes are produced (and the symptoms developed), the less

202 LECTURE XV.

are they influenced by treatment ; and in sudden lesions, as a
rule, no influence is possible. Neglect of this consideration
often brings discredit upon medical men. I have seen many
cases of sudden hemiplegia, due to syphilitic disease of vessels,
in which the patients werissured Stt if they were properi;
treated they would certainly get well; and when, after several
years, there was ahnost no improvement, they were naturally
inclined to think lightly, and sometimes to speak strongly, of
the medical man who had given a prognosis so erroneous.

LECTUEE XVI.

DIAGNOSIS OF THE NATURE OF THE LESION {Contimied) :

SUDDEN LESIONS.

Q-ENTLEMEN, — ^We ppoceed to-day to consider the methods
of reasoning by which we ascertain the nature of the lesion.
It is possible for me to give you, in these lectures, only an
outline of the subject; but an outline may enable you to
understand the principles and method of diagnosis, and even
fix in your minds the most important rules. In the case of
diseases that vary so widely in their character as do those of
the brain, the most essential thing is to have a firm hold
of the methods of diagnosis. It is only thus that you can
hope to be able to deal with the problems that will confront
you. No two cases are alike, and you will often be at fault
if you trust to rules alone, and do not understand the prin-
ciples, on which the rules are based.

In distinguishing between the several lesions, we are
guided in the first instance by certain indications. The first
is the mode of onset of the symptoms ; this enables us to
distinguish between certain groups of lesions. The second
consists of the causal indications, — the presence or absence
of the conditions under which certain lesions occur, or the

I

evidence of a m'mil ar lesion elsewhere in the system,
third is the position of the difiease : certain mortid processes
are more common than others in certain parts of the brain.
A fourth is the character of the symptoms themselves, which
may vary somewhat in the same part of the brain, according
to the natiire of the disease : this variation is sHght at the
onset, and is chiefly available when the course of the disease
can be ascertained or watched. Lastly, other symptoms of
the morbid process outside the nervous system may indicate
its nature, — such as the pj-rexia that attends inflammation.

The first question, then, is the time occupied by the onset of
the symptoms— whether the onset is sudden, acute, or chronic.
By " sudden " I mean the development of the symptoms to
a considerable degree in from a few minutes to a few hours ;
by "acute," an onset that occupies from a dayto two or three
weeks ; by " chronic," one that occupies more than a month.
We are thus able to form a rough classification of the lesions
into three divisions — ^the first comprehending the vascular
lesions ; the second, the inflammatory lesions ; the third, the
chronic inflammations, the growths, and the degenerative
lesions. Cases of intermediate course are met with, but they
can usually be brought without difficulty into one or other
of these types, to which it is convenient to Kmit o\u«elves,
not only for the sake of simplicity, but because they include
nineteen-twentieths of the cases of organic disease. In thus
using the mode of onset as a means of classification, we must
take care that it is the actual onset that we consider. "We
shall have also to notice certain exceptions to the rules laid
down — -exceptions that are, however, rather apparent than real.

We may consider, first, the group in which the symptoms
are sudden in their onset, developing often in a few minutes,
sometimes occupying a longer time — a few hours. Remember,
as a useful working rule, that symptoms of sudden onset,
due to an organic cause, indicate a vascular lesion. They
indicate the rupttire of a vessel or the obstruction of a vessel ;
the former, as we have seen, causing hsemorrhage, the latter
softening. The exceptions to this ride are few. They include
the transient paroxysmal symptoms, such as convulsion or

PATHOLOGICAL DL\GN0S1S. 205

pain, and also inhibitory palsy ; but the last is very rare.
Again, an abscess of the brain may cause sudden symptoms
by its rupture. This is the most important exception to the
rule that sudden symptoms indicate a vascular lesion; but
even here there are often chronic symptoms before the
sudden symptoms that attend the rupture. Moreover, the
symptoms that result from the rupture of an abscess
are more often acute than sudden, according to the defini-
tion that I gave you of the sense in which we use these
words.

We will take, then, the symptoms, such as paralysis, loss
of sensation, etc., the sudden onset of which justifies us in
suspecting the occurrence of a vascular lesion — softening or
hsemorrhage. We have not merely to decide between the
two, but we have, if the lesion is softening, to determine
its form, that is, the nature of the obstruction that has
caused it. The softening may be from the occlusion of an
artery or of a vein. I told you, in the last lecture, the
pathological causes of the various forms of obstruction, but
it may be well for me to put them before you again in the
form of a table.

A. Haemorrhage — ^from rupture.

B. Softening — ^from obstruction,

(a) in an artery — ^from

(1) local thrombosis, due to

{a) atheroma,

(6) syphilitic disease,

(c) blood-state;

(2) embolism,

(b) in a vein — ^thrombosis.

The actual onset may be preceded by premonitory sjonp-
toms. The significance of the presence or absence of these
is limited. They are confined to those lesions that result
from considerable preceding vascular disease — ^to softening
from atheroma and syphilitic disease of vessels; they are
absent in softening from embolism and in simple thrombosis.
In ordinary hsemorrhage, premonitory symptoms, as such,

206 LECTURE XVI.

are also atsent. The miliary aneurisms cause no sympl
until they burst. Any premonitory aymptoms in htemorrhage
are due, not to the cause of the htemorrhage, but to coexist-
ing atheroma, and have no direct relation to the lesion. In
Byphilitie disease and atheromatous softening, the premonitory
symptoms are transient weakness or tingling in the limbs
subsequently paralysed, due to the diminution of the blood-
supply afterwards arrested ; and in each case there may be
headache. In larger aneurisms, previous symptoms are those
of a pre-existing lesion, causing pressure on some structure at
the base of the brain, and are not true premonitory 8\TQptoms.
The presence of premonitory symptoms may be of diagnostic
importance, but their absence is of very little significance,
since thei-e may be none even in the diseases that are moat
often attended by them.

The actual onset is the next element in the diagnosis. The
indication that it affords must ordinarily be used in subordi-
nation to the causal indications. Nevertheless it is important
to consider it first, because it does oooasionally affoi-d a very
strong indication, so decided as to override every other con-
sideration. The chief guiding point is the effect on consoions-
ness — the occurrence of apoplexy, its degree and duration.
Either softening or htemorrhage may cause apoplexy, but it
is produced by hfemorrhage more readily than by softening.
Deep coma, lasting many days, is very rarely caused by
vascular obBtruction. On the other hand, it is not common
for there to be no loss of consciousness in haemorrhage, unless
the extravasation is very small in size. Hence the absence of
this symptom is not of much weight unless there is reason to
think that the lesion is of large size. All that can be said is,
that if there is complete hemiplegia lasting for some days, and
no unconsciousness at the onset, the lesion is more likely to be
softening than hEeraorrhage ; and if there is deep and prolonged
coma, the lesion is almost certainly htemorrhage, unless the
patient is very old, and then there is some probability of
softening, even with prolonged coma. If focal symptoms are
sKght, and initial apoplexy was well marked, hremorrhage is
much more likely than softening.

PATHOLOGICAL IIIAGNOSIS. 207

When tlie onset occupies several hoiire, the Bymptoms
developing gi'adually without initial loss of consciouanesB, we
must wait for the termination of the onset. If it ends in
deep coma (ingravescent apoplexy), there is almost certajnly
haemorrhage. If it ends in a stationary condition, without
any loss of consciousuees, the lesion is probahly softening.

We must consider, next, the causal indications. They
should not he taken in subordination to the mode of onset,
hilt independently. The two should then be compared,
their indications balanced, and their relative weight esti-
mated. The first causal indication is the age of the patient.
Hsemorrhage is so rare under forty, that it wotild not
be auspeefced unless deep coma strongly suggested it. Soften-
ing from atheroma is still more rare under forty. This
renders the diagnostic problem far more simple during the
first half of life, since there remain only three oommon
vascular lesions — embolism, thrombosis from syphilitic disease,
and thrombosis fi-om blood-states. We may conveniently,
therefore, limit oui'selves, in the first instance, to the cases
that occur during this period of life. In each ease we must
begin by searching carefully for any indications of the
presence of one of these three causes, always remembering,
however, that hemorrhage, though not probable, is possible,
even in childhood.

In the last lecture we considered the chief causes of these
lesions, and I told you that embolism, in the vast majority
of oases, is from the heart, and is associated with valvular
The first point to be ascertained is therefore the
ibsence of such disease. In recent cases you are
only justified in suspecting embolism, in the absence of
valvular diseafie, when there is some other condition which
may be the source of a plug (such as an aneurism of the
aorta) . But if the diagnosis has to be made a year or more
after the onset of the hemiplegia, we cannot exclude em-
bolism because we find no indications of valvular disease of
the heart, if the onset occurred during, or soon after, such
an illness as ia usually, or occasionally, attended by endo-
carditis — acute rheumatism, chorea, or scarlet fever, I have

LECTUBE XVI.

known, for instance, mitral endocarditis during chorea to
nauee cerebral emljolisni, and a year later the heart had so
far recovered that no evidence of vahiilar disease could be

There is one exception to the rule that valvular disease in
a young person makes it probable that the lesion ia embolism.
Valvular disease may lead to cerebral hteniorrbage by causing
an aneurism. I told you in the last lecture that the im-
perfect obstruction of an artery by embolism is one of the
most common causes of intracranial aneiu-ism. Hence, if
the initial apoplexy is deep and prolonged, or if there is the
" ingravesceut apoplexy " already mentioned, the presence of
heart disease not only does not exclude hemorrhage, but
increases its probability. This is true, even in children.

In thrombosis from blood-states alone, the causal indication is
usually obtrusive. In adults this influeuce is almost confined
to the post-puerperal condition. The clot may be formed iti
xitii, or, if there is valvular disease, it may be formed, in the
heart, and carried to the brain. In other conditions favour-
ing coagulation, such as phthisis and cancer, the clot generally
forms in a vein. This is true also of the thrombosis that
occurs so readily in young children, of which I spoke to you
in the last lecture. The fact that the patient is very young
and does not suffer from heart disease, or that the attack
octsurs during a state of oonsiderable prostration, j'u^ifies a
diagnosis of thrombosis ; and if the symptoms are those of a
cortical lesion, you may feel confident that the thrombosis is
in a vein.

Thrombosis in an artery, from syphilitic disease of the wall
of the vessel, occurs from six months to twelve years, or even
more, after the primary disorder. In many cases there is a
history of syphilis, and no other cause of arterial obstruction
can be traced. We may then feel sure that a sudden cerebral
lesion is due to this cause. If, however, we have no history
of syphilis — as, for instance, in the case of a patient who is
unconscious, and unable to give us his history, — we have to
rely on the indication afforded by the age, aud on the absence
of other causes. Often we are aided by the presence of pre-

rATHOLOGICAL DIAGN'DSIS.

209

monitory symptoms, suck as headaclie, or slight symptoms in
the Kmbs that are afterwards paralysed. These symptoms
are of especial diagnostic importanoe in cases in which there
is heart disease, and the patient has had aj-philis. We then
have to decide hetween embolism and syphilitic thrombosis.
In the former, as we have seen, premonitory sjonptoms are
absent. Hence, in such a case, any symptoms that suggest
that there waa a morbid process at work within the cranium
before the occurrence of the vascular obstruction, make it
probable that this obstruction is due to thrombosis, and not to
embolism. For instance, a man who had old-standing aortic
regurgitation was seized with hemiplegia. He had suffered
from severe headache for a few weeks before the attack.
Many years before, he had suffered from constitutional syphilis.
The headache that preceded the hemiplegia could not be
explained on the supposition that the lesion was embohsm,
and made it probable that the obstruction was due to throm-
bosis from syphiUtie disease of an artery. Although there
was no opportunity of ascertaining the exact nature of his
lesion, yet it is probable that the diagnosis was correct,
for a few weeks later some nodes appeared upon the skull,
showing that the syphilis was still active in his system.

Syphihs, as well as heart disease, may cause cerebral
hsemorrhage, and by the same mechEinism, by causing an
aneurism. Hence, also, a history of syphilis does not lessen
the probabUity of hiemorrhage, if this is suggested by the
character of the symptoms.

In the second half of hfe, the diagnostic difficulty is far
greater. The causes operative during the first half continue
during the second (although they become less efEective as life
advances) , and, in addition, the potent mechanisms of arterial
degeneration come into operation. Thrombosis from athe-
roma, and hEemorrhage, increase in frequency np to extreme
senility ; then, thrombotic softening becomes more frequent
than hiemorrhage, and is more probable if other indications
are equally balanced.

The most important indications in this period, are those
drawn from the state of the vascular system. Arterial ten-

LECTURE XV:

Bion and a strongly acting heart suggest hiemoirhage ;
soft pulse and an irregular, feeble heart suggest softening.
K these indications are strongly marked, their significance
is very great. Mere arterial degeneration t«lls us httle. It
tells us that the cause of softening exists — atheroma; but
thin so often coexists with the miliary aneurisms that oanse
hteraorrhage, that its significance is small. All that can be
said is, that if other indications are equally balanced, con-
siderable degeneration in the accessible arteries renders
cerebral softening rather more probable than cerebral
hsemorrhage. As we have seen, while atheroma is almost
invariable in senile softening, it is absent in about a quarter
of the cases of hsemorrhage. Advanced Bright's disease
causes both, atheroma and miliary aneurisms. It may thus
be a cause of either softening or hsemorrhage. The former
is, however, a rather more frequent consequence than the
latter, perhaps because the miliary aneurisms attain an effec-
tive degree earlier than does atheroma, unless the patient has
reached the period of senile degeneration. Hence, if other
indications are equal, and the patient is not very old, Bright's
disease suggests hsemorrhage ; but if the other symptoms are
sucli as to suggest softening, their significance is not appreci-
ably lessened by the presence of Bright's disease.

Aa I have said, the difficulty in the diagnosis during the
second half of life is increased by the circunistance that the
vascular lesions common in earlier life — embolism, and throm-
bosis from syphilitic disease — occur during this later period.
Thrombosis from the state of the blood and circulation also
occurs, but the powerful influence of the puerperal state is
no longer effective, and the influence of the circulation in
causing thrombosis becomes to a large extent merged in that
of the arterial degeneration, since it is rarely effective alone.
On account of the frequency of the senile lesions, the mere
presence of a cause of one of the earlier lesions, — a history
of syphihs, or a source of embolism, — is of far less diagnostic
significance than it is during the first Iialf of adult life.
The diagnosis rests, therefore, in larger degree on other
indications than those of a present cause. If such other

PATHOLOGICAL DIAGNOSIS. 211

indications are absent, the diagnosis ia a matter of protability
only, or rather, I should say, of probability that is never
high. All diagnosia that is founded on reasoning, and not
on simple ohBervation, is a matter of probability. "Where
Beveral and different indications coexist, the degree of prob-
ability is often very low. The indications that guide us
correctly in two eases may fail us in the third. A woman of
fifty-five died with symptoms of a vascular lesion. The age
of the patient made it probable that the lesion was either
hismorrhage, or softening from atheroma. Of the two, the
symptoms suggested the latter. But the patient also had
considerable mitral obstructive disease, and this made em-
bolism a possible lesion. After death there was found, as
expected, softening and not haemorrhage; but the soften-
ing was due to syphilitic disease, extensive and characteristic,
of the likelihood of which we had no suggestion from the
patient's history. Dr. HughUngs-Jackson has recorded a
ease in which atheroma and syphilitic disease coexisted, and
softening that had occurred was due only to the former. These
oases illustrate the difficulty in diagnosis that results from
the persistence during the senile period of the causes of
vascular disease that are operative during the first half of
life ; and in such the diagnosis must usually be a matter of
probability only, and of very low probability, and a con-
clusion, rightly reached, may imavoidably be wrong.

The second element in the caueal indication is the evidence
of a lesion elsewhere, of the same nature as that within the
brain — evidence that a morbid process is at work in the
system, such as may be the cause of the cerebral lesion. Most
of the vascular lesions may occur outside the brain, and we
may sometimes detect them. If they occur at the same time,
or about the same time, as the cerebral lesion, they afford
strong evidence of the nature of the latter. The occurrence
elsewhere of the process of embolism may be recognized ; as,
for instance, in the spleen, by the enlargement and tendei-ness
of the organ. The central artery of the retina may be ob-
structed by embohsra, thus affording evidence of this process

p 2

in the arterial system to which the cerebral vessel belongs.
If , as I have aeen, the retioal artery is occluded at the same
moment as the cerebral artery, the evidenoe of the nature of
the lesion in the brain amoimts almost to demonstration.
In syphilis we rarely have a more special indication of the
precise process at work in the brain. Neither syphilitic dis-
ease of vessels, nor thrombosis therefrom, is to be recognized
elsewhere, except in the rarest eases ; but other indications that
the syphilitic vims is still active may furnish equivalent evi-
denoe. Simple thrombosiB, from blood-etate, is occasionally
accompanied by a similar accident ia some other part, espe-
cially during the puerperal period. A clot may form in a
vein of the leg, or some other part. Arterial or venous throm-
bosis elsewhere, from combined arterial disease and feeble
circulation, coincides not unfrequently with cerebral throin-
bosis, and affords presumptive evidenoe of the nature of the
lesion of the brain. Instances are senile gangrene of the
foot, thrombosis in the veins of a leg or of the retina in those
who are old and gouty, or feeble and depressed. Hiemorrhage
elsewhere is rare in cases of cerebral hsemorrhage, except in
the eye, and even there is significant only when the extravasa-
tion is large. The small hcemorrhages in the retina, that are
so common in albuminuria, do not signify more than that
the kidneys are diseased, and afford alone no more evidence
that the cerebral lesion is hemorrhage than does the renal
affection itself. The significance of this we considered before.
A large intra-ocular hfemorrhage, such as one into the vitreous,
makes it highly probable that the cerebral lesion is of the
same nature. But extravasations elsewhere, in the course of a
general disease that is attended with a hsemorrhagic tendency,
such as pernicious anjemia or leucoeythEemia, also afiord
strong reason for believing that a cerebral lesion is of the
same nature.

The position of the lesion occasionally helps us. A lesion
of the pons, and still more of the medulla, that is not quickly
fatal, is much more likely to be softening than hfemorrhage.
The basilar artery is a frequent seat of syphilitic disease, and

PATHOLOGICAL DIAGNOSIS. 213

if other indications axe equally balanced, in a case in which
the symptoms suggest an obstruction of the basilar, as, for
instance, the presence of heart disease and a history of
syphilis, the fact that the basilar is the affected artery would
turn the scale in favour of syphilitic thrombosis, against
embolism. If the symptoms point to a cortical lesion, and
other indica;tions are equally balanced, this is much more
likely to be softening than hsemorrhage. The sudden exten-
sion of the symptoms from one side to both, with renewed
coma, that is produced by the rupture of an extravasation
into the ventricles, constitutes evidence that the lesion is
hemorrhage, and not softening ; but this significaace is only
decided when the extension occurs within a few days of the
onset. Even then it is not a certain indication. Identical
symptoms may attend the formation of a clot in a large
artery of the other side of the brain in cases of softening,
and if such symptoms come on after the first few days, it is
even more likely that they are due to a fresh lesion than to
the extension of the old one, and they therefore no longer
have a definite significance. Hence it also follows that when
there is decided reason to believe that the original lesion
was softening, the occurrence of symptoms like those of
ventricular haemorrhage does not materially weaken the
original diagnosis.

The character of the symptoms, in relation to the position
of the lesion, does not give us much help in the case of acute
lesions. Convulsions at the onset are of little significance.
Those that succeed the onset, or occur during the subsequent
course of the disease, are in favour of the lesion being
softening, rather than haemorrhage. An intense degree of
secondary irritation is in favour of softening. So also are
the athetoid movements, " mobile spasm," that may come
on after the hemiplegia has existed for some months.

Here, for to-day, gentlemen, we may conveniently stop.
There remains for consideration the diagnostic significance of
the symptoms that attend the acute and the chronic lesions.

214 LECTURE XVI.

But the chief acute lesion, according to the classification that
I gave you at the outset, is meningitis. I propose, after we
have completed our survey of the chief diagnostic indications
from the side of the symptoms, to review them from the side
of the lesions. It will be convenient to postpone the con-
sideration of the symptoms of meningitis until we come to it
in that survey. The symptoms that may result from chronic
lesions we will proceed with at our next meeting.

LECTUEE XVII.

DIAGNOSIS OP THE NATURE (Continue) : CHRONIC LESIONS-
SYMPTOMS IN THE SEVERAL MORBID PROCESSES.

Gentlemen, — The chronic lesions of the brain are chronic
meningitis, tumour, aneurism, abscess, disseminated sclerosis ;
and we may include among them labio-glossal paralysis and
general paralysis of the insane. In aU these diseases well-
marked symptoms develope, as a rule, slowly, occupying at
least several weeks, and often several months, in their progress
to a considerable degree of intensity. It is true that one of
them (tumour) occasionally, and two of them (abscess and
aneurism) frequently, have a latent course, and then give
rise to acute and even sudden symptoms. But as pathological
processes, they are chronic, and the symptoms of their develop-
ment, when these exist, are correspondingly chronic in their
evolution.

The first point to be considered in the diagnosis of these
diseases is the causal indication that can be discovered. This
element is rarely of much significance ; it is far less important
than it is in the sudden lesions of the brain.

The age of the patient may afford some guidance, since
general paralysis, chronic meningitis, and aneurism are prac-

216 LECTURE XVII.

tically confined to adult life; aneurism and diBBeminated
BcleroBis being sometimes met with in youth. Tumour and
abscess occur in all ages. Sex helps us only in so far as
general paralysis is rare in females. Heart disease is a cause
of aneurism alone among the chronic lesions. Syphilis may
cause tumour, chronic meningitis, or aneurism. It is by far
the most frequent cause of cerebral tumour in adult life.
Chronic meningitis is very rare as a solitary lesion, and is
due usually either to injury, chronic alcoholism, or to syphihs.
In the absence of these causes it is very improbable.
Injuries to the head may also cause abscess, or, in rare
oases, tumour. The most common other causes of abscess
are adjacent bone-disease, especially in the ear, and sup-
puration elsewhere, especially in the lung. If these are
not present, abscess is unlikely. Tumours are usually
primary, and independent of growths elsewhere. Cancer is
occasionally secondary, and hence a malignant tumour m
some other part of the body renders it highly probable
that symptoms of organic disease of the brain are due
to a tumour. Tubercular growths in the brain are also
occasionally secondary to tubercular disease elsewhere, but
are more often primary, occurring in a subject predisposed
by inheritance to tubercle. Hence either hereditary pre-
disposition or actual tuberculosis suggests that a chronic
disease is a tinnour.

Neurotic heredity, indicated by a history of such diseases
as epilepsy, insanity, neuralgia, etc., is rather agidnst than in
favour of actual organic disease of the brain. Equivocal
symptoms are more likely to be due to functional disease.
Preceding anxiety, or mental shock, also render such dis-
turbance more Hkely than coarse organic disease.

The diagnosis of the chronic lesions of the brain depends
chiefly on the symptoms they produce. Ton doubtless
remember the distinction between the diffuse and the focal
symptoms. The difiuae symptoms, if any are present, are
of much greater importance in the pathological diagnosis
of chronic disease than are the focal symptoms, and we may,
therefore, consider them first. If the symptoms are chiefly

lthological diagnosis. 217

., we have to depend on their mode of development, and
on their confonnity to certain ty^es. An instance of the
latter is the ease of labio-gloseal paralysis, in which diffuse
symptomfi are entirely absent, but the focal symptoms
correspond closely in all cases.

Of the diffuse symptoms we may consider, first, pain in
the head. Headache is a conspicuous symptom in chronic
meningitis, in tumour, and often in abscess. It is absent in
the purely degenerative diseases. In aneurism it is sometimes
marked, sometimes it is trifling, occasionally it is absent.
Remember that the eharacteristica of the pain of organic
disease are severity and constancy, and the association with
other symptoms. One of these is vomitiag, which occurs in
the same lesions as headache, and often coincides with the
more intense paroxysms of pain. Of even greater significance
is the association with optic neuritis. Rare in aneurism, optic
neuritis is frequent in abscess and chronic meningitis, and
most frequent and intense in tumour, in which it occurs, at
some period, in five-sixths of the eases. If there is no cause
of abscess to be discovered, persistent headache, and consider-
able optic neuritis, may he regarded as almost certain indica-
tions that the organic disease is a tiunour. But remember
that the optic neuritis of tumour is not always intense. In
cases of slowly growing tumour, it may be slight in degree,
and extremely chronic in course. Atrophy of the optio nerves
varies in its significance according to its form. "Consecutive
atrophy," that which follows neuritis, has the same signifi-
cance as the neuritis that precedes it. Simple atrophy is rare
except in the degenerative diseases, disseminated sclerosis and
general paralysis of the insane. Its significance is always
that of a degenerative process. Atrophy, that foUoira loss of
sight, is due to damage to the optic nerve, and indicates either
a tumour pressing on the nerve, or inflammation involving it.
Loss of the reflex action of the pupil to hght, without loss of
sight, has the same significance as primary atrophy ; it is due
to degeneration, and indicates that a degenerative process is at
work. It affordsa ground for suspecting that other symptoms
are due to a similar degeneration. It does not prove this. A

i

318 LECTURE XVII.

ooarse disease may coincide with a degenerative proceea. Such
coincidence is now and then observed in syphilis, which pre-
dispoBes to degenerations even during the stage in which it
still causes organic lesions. Nystagmus occurs in tumour and
in some degenerative diseases, hut is not common in either
class, except in disseminated sclerosis ; in this it is a very
frequent symptom.

Mental ehange may have various meanings, according fo
its form. Exaggerated delusions occur chiefly in general
paralysis of the insane, hut the early stage and shghter form of
this disease are often attended by a simple optimism, in which,
without any false idea, all things are looked at in a favourable
light; the patient is happy under depressing circumstanoeH,
and is always "better" or "well" when physical weakness
is steadily increasing. An unnatural complacency, without
actual optimism, is also common in disseminated sclerosis. It
ia often marked, even in the early stage, and is a significant
symptom that should always attract attention. This form
of mental change is oonflned to these degenerative diseases,
and is not met with in other organic lesions. Chronic
delirium, sometimes active but amenable, may occur in
chronic meningitis and tnunour ; nocaaionally the delirious
condition resembles closely that of chronic insanity. More
common in these diseases is simple mental failure — loss of
memory, and slowness of speech — deepening to lethargy.
In a considerable degree of this condition, faeces and urine are
often passed without notice, although there is no paralysis
of the sphincters. I have more than once mentioned to you
the importance of this symptom.

Convulsions are absent in disseminated sclerosis, and also
in most eases of aneurism, until rupture occurs. They are
common in timiour and in chronic syphilitic meningitis, but
not in alcoholic meningitis. They occur also, although not
very frequently, in general paralysis of the insane. In each
disease in which they occur, the convulsion may be general
or partial, the latter form being, as you know, a focal symp-
tom. Shght partial fits, recurring with great frequency, are
almost confined to tumour.

PATHOLOGICAL DIAGNOSIS. 219

Certain focal symptoms need special consideration, because
they cliaracterize certain forms of cerebral disease. Defect
of articulation is produced by any disease of the medulla
and pons, but it is also an early and characteristic symptom
in the degenerative diseases — sclerosis, general paralysis,
and labio-glossal paralysis. In the latter the defect is
dependent on actual loss of power in the lips and tongue,
which can be recognized as soon as there is much impair-
ment of articulation; but in the two former diseases, sclerosis
and general paralysis, there is at first no distinct weakness.
The alteration in the early stage may be very similar in the
two — a tendency to clip words, to run together syllables,
which are thus confluent, instead of being " articulated." As
sclerosis advances, however, there is usually a tendency to
a separation of syllables. The staccato and elisive defect
may coexist (see p. 106). In general paralysis, speech
usually becomes hesitating, and is interfered with by
manifest tremulous twitching of the muscles of the lips
and face; often words are drawled out, and sometimes a
guttural noise accompanies inspiration.

Another important group of symptoms are those of the
eyeball muscles. Any disease at the base of the brain may
paralyse these muscles in one or both eyes, but a slow
progressive palsy, involving many muscles of both eyes,
without other indications of basal disease, shows a progres-
sive degeneration of the nuclei of the nerves, analogous to
that of the bulbar nerves in the labio-glossal palsy.

Of the focal symptoms in the limbs, only one class is of
sufficient pathological significance to need mention. Tremor
is common in general paralysis, but may occur in tumour,
and in chronic meningitis. Jerky inco-ordination of move-
ment, accompanying weakness, is a characteristic symptom
of disseminated sclerosis, but it occurs also in cases of
tumour, chiefly in children (see p. 66).

We may now review these facts from a different side —
from the side of the lesions, — and consider the aggregate

of symptoms which indicate the several leaions, i.e., tte
Bymptoras that these lesions produce in typical cases. In
doing so I shall have to repeat many things that I have
already said. I need not apologize for this, because, gentle-
men, you have failed to leam the most important lesson
in method of study if you object to repetition. Ton can
only leam thoroughly by going over facts many times in
their different relations.

AVe will commence again with the cases in which tlie onset
is sudden, and take first the conditions in which there is loss
of consciousness, apoplexy, but in which there are no indica-
tions of a one-sided lesion. There may be no symptoms on
either side of the body and limbs, or there may be symptoms
on both sides. These symptoms are in the state of the
musdes, relaxation or oontraeture, or in the state of reflex
action. "We may thus divide these cases into two classes,
according to the absence or presence of symptoms of bilat«ral
character.

We will take first the cases in which there are no peripheral
symptoms recognizable on either side. A patient may sud-
denly become uneonseious, and remain so, and may not only
present no indications of damage to one side of the brain,
but there may he such restless automatio movements of the
limbs on both sides, as indicate with certainty that there is no
damage to the motor tract of either side. In most cases of
the kind the coma is incomplete — there is stupor rather than
coma. The patient, usually between forty and sixty, is i)f
plethoric aspect, the pulse full, the carotids pulsate strongly,
the face is flushed, reflex action is normal, tbe pupils are of
medium size and act to Hght. In the course of two or tbi'ee
days the symptoms pass away entirely, and no indicatitm
of any focal lesion can be found, when consciousness has
returned, and a thorough investigation is possible. Such an
attack is probably due to cerebral congestion. It is custom-
ary to ascribe it to this cause, and the balance of evidence
is in favour of the correctness of this opinion. The patient
often has more than one attack of this character.

In the second class of cases the apoplexy is aooompanied by

PATHOLOGICAL niAnXUSIS.

2a 1

evidence of interference with the motor centres on hoth sides
oi' the brain. There is either complete relaxation of the
miiHolea, or hilat«ml rigidity, or rig;idity in Bome parts and
resolution in others. In these cases we have to deal with a
lesion either in or o\if«ide both hemispheres or in the pons.
There may be ventricular haemorrhage, meningeal haemor-
rhage, obstruction of vessels in both hemispheres, hEemor-
rhage into the pons, or softening of the pons. If imiversal
reaolution and deep coma succeed, after a few hours or a day
or two, the following symptoms— mental excitement, rigidity,
convulsive movements (now in one part, uow in another), and
sudden headache — there is probably meningeal hcemorrhage,
and this is especially probable if the symptoms succeed an
injury. If, in a patient under forty, with heart disease or
old syphilis, the coma is complete from the first, the limbs
relaxed, and the s3nnptoms continue for some hours without
diminution, a cerebral aneurism has probably burst. Head-
ache, giddiness, or palsy of cranial nerves for some weeks or
months before the onset, makes this diagnosis still more
probable. If initial coma is accompanied by indications of
a one-sided lesion, rigidity or resolution of the limbs of one
side, deviation of the head and eyes, followed in a few hom-s
or a day or two by similar symptoms on the other side,
without special affection of the cranial nerves, but with deep
ooma, the lesion indicated is ventricular hiemorrhage. If the
symptoms are from the first bilateral, if there is rigidity or
resolution, or the two are associated in different parts, if there
are convulsive movements in both arms or both legs, inter-
ference with respiration within two or three hours of the
onset, strong contraction of the pupils persisting or yielding
to wide dilatation, a rise of temperature to 102° or more
within an hour of the onset, the indication is hEemorrhage
into the pons. If, however, similar symptoms come on
gradually in the course of one or two days, the coma at first
incomplete, and slowly deepening, without any early rise in
temperature, with irregular affection of the cranial nerves,
recognizable before the coma becomes deep, the indication is
an occlusion of the basilar artery. Whether this is due to

322 I,ECTUBE XVII,

embolism or thromboBiB must depend on the 3
onset in the former, and on the causal indictitiona. lu
the one caBe a source of eniboliBra will be found, and perhaps
indications of embolism elsewhere. In the other case these are
absent : syphiUs may be probable or certain ; or the patient is '
in the deg^enerafive period, with atheromatous arteries and a
weak heart.

We will take next tbfe case in which a patient is seized with
apoplexy, and there is distinct evidence of a one-sided lesion —
relaxation of muscles, loss of the skin reflex, change (loss or
early excess) of the muscle-reflex action, deviation of the
head and eyes. Yon are sure that a vascular lesion has
occurred, on account of the suddenness of the onset ; and un-
!■ less the patient is a child, or is suffering from phthisis or

[I other cause of extreme weakness, you are sure that it is an

arterial lesion — an artery has given way, or become stopped
up. For further guidance you examine the pulse, arteries,
heart, and urine. At any age, after childhood, deep coma,
lasting many hours, renders hsemorrhage probable, the more
so if the patient is over thirty-five, and is suffering from
Bright's disease. The significance of pralonged coma as
an indication of hEeraorrhage is much greater in early
and middle life than it is in old age, since in the latter it is
produced by arterial occlusion much more readily than in the
former. Mind, I am speaking of actual coma, not of the
mere hiatus in conscious memory, which the patient afterwards
describes as nnconsciousness. He may tell you of a period
of unconscionsness lasting for many days, when what we
term manifestations of eonscioxisness returned in a few hours.
The indications afforded by the prodromata, onset, pulse,
arteries, and heart, I have already described, and need not here
repeat, beyond reminding yon that embolism is suggested by
valvular disease of the heart, especially during the first forty
years of life, by a sudden onset without prodromata, by the
brevity or absence of initial loss of consoionsness, and by the
evidence of eraboHsm elsewhere. Syphilitic disease is sug-
gested by a history of syphihs, or, failing this, by its possibility
combined with the absence of other causes, by the ocourrenoe

U

PATHOLOGICAL DIAGNOSIS. 223

of prodromata (headache, symptoms in the limbs afterwards
paralysed), by an onset that is sudden or deliberate, but with-
out, or with only brief, loss of consciousness. Hsemorrhage
is suggested by the degenerative period of life, — ^but is not
absolutely excluded even by youth ; by deep and prolonged
coma, — ^but is not excluded by brief coma, or even by the
absence of any loss of consciousness. It is suggested also
by high tension of pulse, a strongly acting or hjrpertrophied
heart, the absence of prodromata, an initial fall of tempera-
ture, and the presence of Bright's disease. Softening from
atheromatous thrombosis is suggested by the degenerative
period of life, and, unlike haemorrhage, is excluded by youth
or early adult age. It is further suggested by a dilated,
feeble, and especially an irregular heart, by previous slight
attacks of the same nature, by prodromata in the limbs after-
wards paralysed, by the brevity of initial coma, and a fortiori
by the absence of loss of consciousness at the onset.

Simple arterial thrombosis, from the blood-state alone, may
be suspected if there is a constitutional state known to favour
thrombosis, especially the puerperal state, and if no source of
embolism can be discovered, and no cause of arterial disease
can be traced.

Venous thrombosis is suggested by previous profound
prostration and weakness, and especially by the patient being
an adult in the last stage of phthisis, or a child under five
years of age, and by the occurrence at the onset of convul-
sions in, or beginning in, the limbs afterwards paralysed, —
convulsions that indicate a cortical lesion.

Sinus-thrombosis is indicated by somnolence increasing to
coma, and attended by general convulsions, coining on in a
young child prostrated by diarrhoea or some other exhausting
diseiase, or in a patient who has external disease adjacent to a
sinus. In the latter case, focal symptoms may be present,
which vary according to the sinus occluded. The diagnosis
is only certain, however, when external tumefaction near the
position of the sinus succeeds the other symptoms.

The indications that I have given you hold good, not only

224 LECTURE XVII.

of hemiplegia, but also of other symptoms of an organic
lesion, hemianaesthesia, hemiopia, and the like, which cannot,
as a rule, be recognized until initial loss of consciousness has
passed away.

We may now pass to the chief acute lesion of the brain —
meningitis. The symptoms that should lead you to suspect
meningitis are the combination of headache, vomiting with-
out gastric cause, pyrexia, and delirium coming on in an
acute manner. Remember that the absence of any one of
these is of little negative significance. Headache is, how-
ever, seldom absent, and perhaps is never absent at all
periods of the case, but is sometimes only trifling at the
onset. On the other hand, it is usually severe, and the
leading symptom. Remember, also, that the presence of
only one of these symptoms is of no significance, and that
this is true also of the combination of two of them — delirium
and pyrexia, — ^which, without other indications of brain nns-
chief, suggest a general and not a cerebral disease. The
addition of moderate optic neuritis, of inequality of pupil,
strabismus, palsy of cranial nerves, however slight, rigidity
or weakness of limbs, retraction of head, or convulsions, adds
very much to the probability of the diagnosis.

The diagnosis of the nature of meningitis is often less
easy than the recognition of its existence. A family history
of phthisis, or the presence, in an adult, of actual lung disease,
suggests the tubercular nature of the inflammation, as,
indeed, does the mere circimistance of childhood or youth,
in which tubercular meningitis is far more common than
any other variety. The absence of a cause of another form
of inflammation is also an important negative element in the
diagnosis. The indications of the other forms of meningitis
are chiefly causal. Purulent inflammation may be suspected
if the symptoms of meningitis follow suppuration elsewhere,
near or distant, or signs of general septicaemia. The causes
of purulent meningitis and of cerebral abscess are for the
most part the same, and when an abscess causes acute symp-
toms, the diagnosis between the two is often difficult. It

PATHOLOGICAL DIAGNOSIS. 225

depends chiefly on the greater affection of the cranial nerves
in meningitis, and on the history of previous more chronic
cerebral symptoms in abscess. But it must be remembered
that an abscess and purulent meningitis not unfrequently
coexist.

In this outline of the most important symptoms of the
sudden and acute lesions, I have said nothing of ansemia of
the brain, because it is extremely rare for symptoms due to
this cause to come into any diagnostic problem. Almost the
only cases in which such symptoms are important are those of
young children who are profoundly exhausted by diarrhoea.
The patient may become somnolent and comatose ; may some-
times present convergent strabismus, and even rigidity of the
neck. These symptoms may pass away ; or the comamay deepen,
the pupils dilate, and the child die — ^the brain after death
presenting no morbid change. The state was called " hydro-
cephaloid " by Marshall Hall from its resemblance to menin-
gitis, which is sometimes called " acute hydrocephalus." The
diagnosis from meningitis depends on the absence of focal
symptoms and on the circumstances under which the symptoms
came on. The distinction from sinus-thrombosis is still more
difficult, and depends chiefly on the depression of the f ontanelle,
the absence of external tumefaction, and of limb-symptoms.
Often, however, it is necessary to wait before a confident
opinion can be given.

Q

DIAGNOSIS OF THE NATITKE OF THE LESION (CoiUinutd) :
SYMPTOMS PRODUCED MY CHRONIC LESIONS, TUMOUR,
ANEURISM, ABSCESS, DEGENERATIVE DISEASES— DIAGNO-
SIS BETWEEN FUNCTIONAL AND ORGANIC DISEASES-
CONCLUSION.

GrENTLEMENi^In the last lecture we commenced a survey
of the groups of symptoms that mdieate special lesious of
the brain. We considered those that characterize the chief
morhid processes that are suddeu and acute. We pass now
to the symptoms that attend the chronio lesions of the brain —
chronic meningitis, tumour, aneurism, abscess, and the degene-
rative processes that we decided to include in our survey.

Chronio meningitis need not detain us long. The alcoholic
form occupies the convexity, and causes diffuse symptoms,
especially headache and delirium. Occasionally there is
slight optic neuritis. It is probable that the inflammatory
changes found in the membranes are part of a slight
general encephalitis, rather than the actual cause of the
symptoms. Syphilitic meningitis differs from all other forma
in being local and never general. Hence its symptoms closely
resemble those of a syphilitic growth. A positive diagnosis

.4

PATHOLOGICAL KIAGNOSIS. 227

between the two is rarelj possitle, and indeed they frequently
coexist. The chief difference is, that in meningitis the
sj-mptoms of irritation are greater than ie the evidence of
destruction, and the symptoms indicate a wider extent of
mischief, especially at the base, than a growth would be likely
to produce.

The symptoms that suggest the existence of a tumour are
severe and persistent headache, vomiting, and optic neuritis,
with progressive sjTnptoma of interference with the functions
of some part of the brain. These must be searched for, in
every ease, most carefully. Many of the most important are
unnoticed by the patient. The pupils should be compared,
their action to light ascertained. The movement of the eyes
in every direction should be observed, and if there seems to
be any defect, a coloured glass should be used to examine for
double vision. The hearing should be tested, the strength of
the masseters felt, the movements of the tongue and palate,
and the closure of the vocal cords should be tested by
making the patient cough. The voluntary, emotional, and
associated movements of the face should be carefully observed.
In the limbs and trunk the reflex action should be especially
examined, A loss of the superficial reflexes in limb and
trunk is sometimes the first objective symptom of tumour on
one side. If there is evidence of the existence of a tumour,
the next question is, Is the growth in and invading the brain,
or outride the brain and compressing it? Optic neuritis
is produced more readily by tumours in than by those outside
the brain. If the symptoms indicate a growth of some size
at the posterior part of the base, or over the convexity,
and there is no optic neuritis, this is in favour of the
growth being outside the brain. If the symptoms are those
of a tumour of the pons, and the cranial nerves suffer before
the limbs, and on one side before those on the other, the
tumour is probably outside the pons, springing from the
membranes in the posterior fossa of the skull.

There Btdl remains one of the most diiBcult problems in
cerebral diagnosis. What is the nature of the tumour ? The
answer to this question can sometimes be given with a high

q3

degree of probability, now and then with certainty. Often,
boweTBT, the probability is so low that the answer is hardly
more tban a guess. The chief indications are aa follows : —

(1) The presence of morbid growths ekewhere, the nature of
which can be detennined. If tbe symptoms succeed a cancer
or sarcoma elsewhere, it is practically certain that the intra-
cranial growth is of the same nature. In rare eases the
presence of an hydatid tumour elsewhere Justifies the con-
clusion that the gi-o\vth in the brain is of the same character.

(2) Evidence of a general disease, of which an intracranial
groAvth is known to be an occasional manifestation. Such
diseases are tubercle and syphilis. In adulfa, signs of
phthisis usually precede a tubercular tumour of tbe brain ;
in children there may be no other present indication of
tubereulosifl. A family history of tubercular or serofulous
disease is usually to be obtained. A physical configuration
such as often coexists ■with a tubercular tendency is also
suggestive. The symptoms or history of syphilis, congenital
or acquired, render it highly probable that a tumour is
syphilitic. The absence of a history of constitutional
syphilis, if. tbe patient has had a chancre, should not receive
too much weight, since secondaiy symptoms are often
imrecognized, or even absent. Moreover, in an adolt,
the sypbilitio natiu"e of a growth cannot be excluded
unless we can exclude the possihilifij of infection, since
even the primary disease may have been unnoticed, aa
in many cases in which constitutional syphilis is patent.
These diathetic indications afford a probability of the nature
of tbe growth — often a very high probability, btit no more
than a probabihty, since a cerebral growth of other nature
may coexiBt with either diathetic state. (3) The age of tbe
patient affords a little help. If the patient is under fifteen,
and presents no indication of inherited syphilis, the tumour is
not a syphiloma. If the patient is an adult, and presents
no indication of phthisis, tbe tumoiir is not likely to be
tubercular. (4) The seat of the disease may give some
assistance. In the cerebellum or pons, a tumour is likely
to he tubercle or glioma, or, also if in tbe pons, it may Iw

PATHOLOGICAL DIAGNOSIS. 229

syphiKtic. A cortical tumour, with signs of irritation, is
probably syphilitic or glioma. A tumour of the base is
probably syphiloma or sarcoma. A tumour outside the
brain-substance is probably a sarcoma. (5) The course of
the growth may be suggestive. A very slowly growing
tumour is not likely to be syphilitic. A tumour that grows
rapidly at the onset, and then becomes stationary, is probably
tubercular or syphilitic. The occurrence of an apoplectic
seizure of moderate severity, with sudden symptoms, is rare
except in glioma. (6) Evidence that arrest and retrocession
of the growth follow the administration of iodide of potas-
sium or mercury is strongly in favour of the syphilitic nature
of the tumour. If these drugs are without influence, and arrest
follows a tonic treatment, the growth is probably tubercular.
(7) Lastly, tubercle, glioma, and syphiloma are the most
common forms of growth in the substance of the brain.
There is always* an intrinsic probability, therefore, that a
growth will be one of these, and this may be allowed
weight in the absence of other indications. Neither the
intercurrent meningitis nor multiplicity of growth is of
diagnostic significance. By a careful comparison of these
considerations a probable diagnosis can be made in a large
number of cases — ^that is, a diagnosis which will turn out more
often to be right than to be wrong.

The symptoms that indicate the presence of an abscess of
the brain are, for the most part, the same as those of tumour
— ^headache, vomiting, optic neuritis, mental dulness, and
focal symptoms. The latter are absent, however, far more
frequently in abscess than in tumour, on account of the great
frequency with which the abscess occupies the temporo-sphe-
noidal lobe, and on accoimt of the tolerance the nerve-elements
exhibit to the pressure of a slowly increasing encapsuled
collection of pus. The distinction depends on the course and
associations of the cerebral symptoms, and on the causal in-
dications. (1) Instead of the uniform progress of the sjrmp-
toms of a growth, those of abscess are for a long time slight
in what is termed the " latent stage.'' They then develope

230 LEC-ITRE XVlll.

rapidly, in an aeiite manner, lite meningitis, or even in a
sudden manner, like hEemorrhnge, distinguiBhable from these
by the definite I'haracter of the slighter chronic symptoms that
preceded. (2) The ophthalmoscope is often of great value,
reveahng, during the latent stage, or at the onset of the acute
stage, nn optic neuritis, which excludes alike a mere vascular
lesion and a commencing meningitis. (3) The general symp-
toms that attend suppuration — fever and rigors— are often
preaeiit. (4) A cause of absoesa (ear disease, suppuration about
the sknll or elsewhere, or an injury) can be found in most
cases. With no cause ascertainable, and an absolute latency, an
abscess can be suspected only on the indication afforded by the
ophthalmoscope. There is no other cerebral lesion in which the
patient may plunge, in a few hours, from apparent health into
imminent danger, and in which considerable optic neuritis is
found at the onset of the acute sjTnptoras, when there is no
general disease to which the optic neuritis can be due.

The symptoms of a small tumour at the base of the brain,
in the position of a large artery, occurring in a person who
is past middle hie, or who has heart disease or syphilis, and,
in the latter ease, not yielding to treatment, justify a sus-
picion of the existence of an aneurism. The suspicion can only
be raised to absolute certainty by the presence of a rare sign,
a murmur audible on auscultation of the skull, practically met
with only in aneurism of the internal carotid. The diagnosis
of the precise artery affected depends on the local symptoms.
I may mention a few of these indications, obtained by
comparing the symptoms in many I'ecorded eases. Optic
neuritis is occasionally met with, hut is not common unless
the aneurism is adjacent to the optic nerve, i.e., is of the
internal carotid or anterior cerebral. The seat of pain is of
significance only when occipital ; it then points to the
basilar as the artery affected. Loss of sight of one eye,
sometimes extending to the other, with, or still more
without, optic neuritis, with or without loss of smeU on the
side first affected, occurs in aneurism of the internal carotid
and anterior cerebraL The distinction between the two

PATHOLOGICAL DIAGNOSIS. 231

depends on the occurrence in the former of paralysis of the
motor nerves to the eye first affected. Paralysis of the third
nerve without affection of sight, or with hemiopia, is produced
by aneurism of the posterior communicating, and also, usually,
with hemiplegia of the opposite side, by aneurism of the
posterior cerebral. Affection of the fifth nerve alone is of
little significance, but with bilateral weakness in the limbs,
and difficulty of articulation or swallowing, it occurs in
aneurism of the basilar. Paralysis of the cranial nerves
below the sixth, associated with weakness of the limbs
on one side, may be due to aneurism of the lower
extremity of the basilar or of the vertebral, and symptoms
of bulbar paralysis, of slow or sudden onset, may occur
in the same cases. Slight hemiplegia is of little sig-
nificance, but, if it is considerable, there is not likely to be
an aneurism of either the anterior cerebral or posterior
communicating artery. Simple general convulsions are very
rare. If they begin locally, they suggest that the aneurism
is of the middle cerebral artery, on the outer surface of the
brain, and if they are opisthotonic, that it is of the basilar.
All these symptoms are, of course, only significant in the
presence of a cause of aneurism. The severe apoplectic
symptoms which attend rupture increase much the probability
of the diagnosis ; but this is then a matter rather of scientific
curiosity than of practical importance. Without preceding
symptoms, the rupture of an aneurism may be suspected if
sudden and deep apoplexy occurs in a person who has not yet
reached the degenerative period of life, and has no renal
disease, and especially if there is heart disease or a history
of syphilis. If the apoplexy is attended first with unilateral
and then with bilateral symptoms, the aneurism that has
ruptured is probably of the middle cerebral. Symptoms of
haemorrhage into the pons suggest that the aneurism is of the
basilar or of the posterior cerebral.

There remain the three degenerative diseases that stand
to some extent, apart from the other lesions of the brain
— ^bulbar paralysis, disseminated sclerosis, and general para-

LECTLRE XVIII.

lysis of the insane in so far as its physical e
concerned. An alteration in articulation is constantly an
early symptom of the first, occasionally of the second, and
frequently of the third. Tremor is a usual symptom of the
two latter, but is absent in the former. In all, the symptoms
are gradual in development, although chronic bulbar para-
lysis has its acute homologue, which depends on a sudden
vascular lesion in the medulla. Although the resulting
symptoms of the acute and chronic disease may be the same,
the sudden onset takes the cases out of the present category
of chronic lesions.

A defect in articulation, and afterwards in swallowing, de-
pending on actual distinct loss of power in the parts concerned,
is the distinctive characteristic of bulbar, or labio-glossal para-
lysis. I told you (p. 107) that the palsy is arranged around the
tongue as a centre, affecting the lips, tongue, palate, pharynx,
and often the lar3Tix ; and I described to you the symptoms
that result. The ultimate aspect of the patient, with motion-
less tongue, open mouth, immobile lower face, and unmodu-
lated phonation on an attempt to speak, is characteristic and
unmistakable.

The distinctive symptoms of insulai- sclerosis are not specially
cerebral. There are coarse jerldugs in the arms, sometimes
in the legs, occurring on movement only. They apparently
depend on the development of islets of sclerosis in the
motor tract, either within the brain or within the spinal cord,
and axe often followed by actual loss of power. Sometimes
unsteadiness on the legs is one of the earliest symptoms.
"With these, however,, are often associated symptoms that are
distinctively cerebral. (1) A change in articulation, in which
syllables are unduly marked ofE from one another, and even
separated, and, at the same time, the endings of words are
slurred. But with this there is no loss of power in the
muscles concerned in articulation, at any rate until the latest
stage of the disease. (2) Nystagmus. (3) A sHght and
inconstant degree of mental change. There may be at first
some mental hebetude, but the most characteristic condition
is an unnatural cheerfulness, and contentment with a state

PATHOLOGICAL DIAGNOSIS. 233

of disability which should naturallj give rise to grave con-
cern. The change never goes beyond this ; but in this degree
it is very common, and rarely fails to strike a medical observer
as peculiar, although the friends regard it as merely the
expression of an admirable resignation.

The early symptoms of general paralysis vary much.
They may be mental or physical. The mental change that
is most characteristic is the familiar "expansive delirium,"
as it is called, in which the patient revels in exaggerated
personal delusions. Often, however, there is no more than a
tendency to regard all things through rose-coloured spectacles,
without any actually false idea. There liay not even be this
optimism ; there may be merely mental weakness and failure
of memory. The physical symptoms are as much spinal as
cerebral. Tremor on movement is often conspicuous ; it
interferes with the more delicate actions, and is especially
conspicuous in the muscles of the lips and face in articula-
tion. Speech is hesitating and drawling, with a tendency to
slur word-endings. Loss of the light-reflex of the iris, and
inequality of the pupils, are common. With these there may
be no spinal symptoms, or there may be indications of either
lateral or posterior sclerosis. Cases of what may be termed
" pseudo-general paralysis," in which the characteristic physi-
cal symptoms exist almost alone — ^merely loss of memory and
slight optimism representing the mental disturbance — are
not imcommon, both in syphilitic subjects and in those who
have not had syphilis. These cases run a much more benign
course than does the classical form of the disease, often re-
maining stationary for years, and even improving. They
do not get into asylums, and therefore are scarcely recognized
in descriptions of the disease, although they are far from rare.

In conclusion, we may glance briefly at some of the more
salient points in the all-important distinction between the
so-called functional and organic diseases of the brain. The
diseases that most frequently give rise to difficulty are
hysteria, neuralgia, and some forms of epilepsy, but the chief
diagnostic indications of the inorganic head-pain and con-

26i LECTURE XVItl.

vulsion have been already alluded to, and I need only now
speak of the often perplexing symptoms of hysteria.

There are few organic diseases of the "brain that the great
mimetic neurosis may not simulate. Palsy and spasm, coma
and convulsion, pain of every form and degree, giddiness,
loss of sight, of hearing, of speech, — almost every symptom of
positive lesion finds its counterpart in the repertoiy of that
functional disturbance which lies, latent or manifest, within
the potentialities of the nervous system of most womai,
and of many men, ready, in some, to spring into activity
on the slightest touch of favouring circumstance. To lead
you fhroTigb the labyrinth of detailed distinction would
occupy as many lectures as we have been able to devote to i
our entire subj(?ct. I must content myself with a briefer j
course— a course, indeed, that may perhaps be more useful to f
you, — and merely point out the general principles that must J
guide you. First remember this fact. Given the condition J
of age and sex — that is, of state of nervous system, develop- J
mental or other — that underlies hysteria, its manifesta-l
tions may be evoked by any disturbance of nerve-function, I
whether this comes from without, as in the pure and primary
disease, or from within, as in secondary hysteria, which may
accompany almost any organic disease of the brain. I
mentioned to you in a previous lecture how many orgimie
maladies of the brain may evoke symptoms of hysteria.
Therefore, given symptoms of hysteria, we must never infer
that this is the primary disease untQ we have searched
for, and excluded, the symptonis of organic disease. A
forfiori this is true of the mere conditions in which
hysteria occurs, and yet the diagnosis of hysteria is often
made merely because the patient who presents symptoms
of organic disease happens to be a girl. The slightest
unequivocal symptom of organic disease is of absolute dia-
gnostic significance, and imtil the absence of any symptoms
of the kind has been ascertained, no other symptoms and
no etiological circumstances should be permitted to bias the
observer's mind. In a large number of c€ises, attention to
this rule will dispel all difficulty. But there remain cases

PATHOLOGICAL DIAGNOSIS. 235

in which the only symptoms present are equivocal, and seem
compatible with each disease, although not characteristic of
either. This difficulty is usually rather apparent than real.
The symptoms common to the two classes present differences
of detail and grouping, and a thorough knowledge of the
characters of organic disease enables the observer to discern
these differences without difficulty. In the very rare cases in
which the symptoms are absolutely equivocal, the history of
other imequivocal symptoms of hysteria may be allowed weight
and to turn the scale. For instance, a lad, after a period
of excessive study, was suddenly seized with severe pain in the
head, which lasted for a day or two, and then gave place to
a state of stupor, in which he could only be partially roused
to slowly swallow nourishment that was placed in his mouth.
The condition resembled that of meningitis ; but a similar
condition is sometimes of purely functional origin. All
other symptoms of organic disease were absent, and it was
ascertained that the headache was preceded by a period of
excessively frequent breathing (a characteristic hysterical
sjrmptom), which ceased suddenly when the headache came
on. This justified a diagnosis of hysterical stupor, and
two days after the onset the lad woke up free from any
serious symptom.

It may be well to glance very briefly at the differences
between some of these equivocal symptoms. Speaking gene-
rally, this hysterical character is suggested (1) by their
onset after emotion, or after witnessing analogous sjrmptoms
in another. (2) By their increase on attention, and in the
course of exanjination. (3) By their mutability; grave
symptoms of one character will cease suddenly, and give
place to others which could not result from the same organic
cause as the first. (4) By the differences between the symp-
toms of hysterical origin, and the corresponding symptoms of
organic disease. For instance, we may take the one-sided
motor palsy of hysteria — hemiplegia. There is rarely com-
plete paralysis in both limbs, although there may be in one.
The face is never affected — an important distinction. There
is usually some contracture in the most paralysed limb, and

this, in the hand, involves tisually the long flexor, flexing a
the phalangeal joints (the metaoarpo -phalangeal more than
in late rigidity), and the flexion of the wrist does not relax
the other joLnts as it does in organic diaease. Moreover,
all hysterical contractures present a distinguishing oharacter-
iatic : when an attempt is made to overcome them, it is felt
that the resistance is not uniform, hut varies from moment
to moment. When the paralysis is incomplet-e, movement
is alow, and is attended by ctiaraeteriBtic irregular tremor,
far smaller in range than that of disseminated sclerosis, but
coarser than simple tremor, and more irregular. If the
muscles are felt or watched, it ■will be found that voluntary
movement is interfered \vith by undue contractions in the
opponents of the muscles that should effect the movement.
There is no wasting, or change in electrical irritability, except
after long disuse, and then only in trifling degi-ee. The
skin-reflexes are not lessened on the affected side ; the knee-
jerts are equal; there is no uniform foot-clonus (unless there
is great contraoture of the calf -muscles) , but what I have
termed a " spurious clonus " can occasionally be obtained,
characterized by the palpable variations in the half -voluntary
contraction of the oalf-mu3cle on which it depends * The
onset of hemiplegia may be rapid, but it is rarely so sud-
denly complete as in organic disease, and is not attended by
loss of consciousness. Anaesthesia is common, either one-
sided and complete, or chiefly localized in the moat paralysed
limb. HemiauEesthesia, coming on without other indications
of a cerebral lesion, is almost always of hysterical origin.

The only derangement of the eyeball-movements that
occurs in hysteria is convergent strabismus from muscular
spasm, and it is easy to observe the absence of any paralysis
if you make the patient, with one eye closed, move the other
in various directions. Simidated ptosis is sometimes seen ;
it depends on a very gentle contraction of the orbicularis,
that is transformed at once into a vigorous and demonstrative
contraction, to keep the eyelid down, if the patient is made
to look up with the other eye.

' See "Diagnosis of Diseases of the Spiiml Cord," Srd Bd.

PATHOLOGICAL DIAGNOSIS. 237

The well-known aphonia of hysteria, depending on
nnder-action of the adductors of the vocal cords, is suffi-
ciently distinguished by the absence of any attempt at
phonation. This inactivity may extend to the tongue, and
cause loss of even whispered speech, a sequence that is
pathognomonic. Very rarely a palsy of the abductors
may give rise to inspiratory stridor without impairment
of expiratory phonation. The symptoms are those of the
same palsy when of organic origin, but the association of
the two is always sufficiently diagnostic. The convulsive
attacks of hysteria ought not to cause a difficulty in diagnosis.
These features are, for the most part, distinctive, and the
problem is, not whether they indicate organic brain-disease,
but whether any other symptoms of a different character
coexist with them.

Here, gentlemen, we must end. The problems that we
have considered in these lectures are certain to present them-
selves before you, frequently, in your future work. Their
form will vary, but the principles of diagnosis that I have
endeavoured to put before you, will guide you, I believe, to a
right conclusion in most cases. When you meet with special
difficulty, do not be hasty in trying to arrive at a decision.
Think over the symptoms ; read over the description of thjB
diseases between which the diagnosis lies; examine your
patient again ; and, if necessary, watch the symptoms for a
time. Perplexing as these problems often are, they are rarely
insuperable to those who combine, with a firm grasp of the
methods of diagnosis, a fair knowledge of the symptoms of
organic diseases of the brain.

INDEX.

-••-

Abduceus nerve, 31

(See also Sixth nerve)
Abductor paralysis of vocal cords, 100
in hysteria, 237
(See also Larynx)
Abscess of brain, 200
symptoms of, 229
Accommodation, centre for, 29

loss of, 89
Acute lesions, 204, 223
Adductor paralysis of vocal cord, 101

(See also Larynx)
Age, diagnostic significance, 204
in sudden lesions, 207
in chronic lesions, 215
Albuminuria from brain disease, 157

significance of, 210
Albuminuric retinitis, 114, 162
Alcoholic delirium, 115

poisoning, diagnosis from apoplexy,
114
Alternate hemiplegia, 58
Amaurosis, sudden, 114
Amblyopia, causes, 74, 75

crossed, 22, 69
Amnesia (see Memory)

verbal, 128, 134
Anaemia, local, of brain, 46

pernicious, hemorrhage in, 212
Aneurism, intracranial, 188
symptoms, 230
miliary, 188
retinal, 162
Aphasia, 71, 127

Aphasia, amnesic, 134
in migraine, 71
motor, 129
sensory, 135
Aphonia, hysterical, 102

diagnosis of, 237
Apoplexy, 110
diagnosis, 112
ingravescent. 111, 207
serous. 111
significance, 206
simple, 110
temperature in, 111
Arterial tension, significance, 209
degeneration, 210
(See also Atheroma)
Arteries of the brain, 38
atheroma of, 188
syphilitic disease of, 188
Articulation, affections of, 105
relation to speech, 122
symptoms in, 219
Atheroma, 188

causing thrombosis, 191
softening from, 192
symptoms of, 223
Athetosis, 60

Atrophy of auditory nerve, 96
olfactory nerve, 72
optic nerve, 74, 165
Attention intensifying sensations, 118
Auditory centres, 25
nerves, 25
irritation of, 97

240

INDEX.

Auditory nerves, nucleus of, 28
paralysis of, 95
speech-processes, 123
vertigo, 148
Aural deafness, 95

vertigo, 148
Automatic movements, escape n
hemiplegia, 53
speech, 125
preservation of, 128

Basal ganglia, 35

(See also Central ganglia)
Base of brain, lesions in, 183
Basilar artery, 41

symptoms of occlusion, 221
Brain, cells of, 2
arteries of, 38
circulation in, 37
veins of, 41
Bright's disease, diagnostic significance,

210
Bulbar nerves, 94
paralysis, 107
acute, 178
chronic, 232

Capsule, internal, 14

anterior portion of, 32

symptoms of disease, 174
Cardiac centre, 28
Caudate nucleus, 35

(See also Corpus striatum)
Cells, nerve, diversit}', 2

in cortex, 8
Central ganglia, 35

arteries of, 38
Central region of cortex, 10

symptoms of disease in, 171
Centre, use of term, 5

motor, 10

speech, 124
Centrum ovale, 8

symptoms of disease in, 173
Cephalic sensations, 144
Cerebellar gait, 36, 179
Cerebellum, arteries of, 41

central ganglia, 35

Cerebellum, connection with cerebrum,
32
functions, 36

hemisphere, disease of, 173
. middle lobe, 36

symptoms of disease of, 179
middle peduncle, symptoms of
disease of, 179
Cheyne-Stokes breathing, 110
Chiasma, optic (see Optic nerve)
Choked disc, 164
Chronic lesions, 215
Ciliary muscle, centre for, 29

(See also Accommodation)
Circulation in brain, 37

in relation to that of eye, 165
Clonus, 54

Colour- vision (see Vision)
Coma, 109

hysterical, 113, 234
ursemic, 114
Compensation, functional, 45
Compression, symptoms due to, 46
Congestion of brain, 186

symptoms of, 220
Congestive attacks in general paralysis,

155
Conjugate deviation of head and eyes,

53
Consciousness, loss of, 109

state in convulsions, 62
Contracture, hysterical, 236
Convulsions, 61

from anaemia, 47

disease of cortex, 171
general, 62
hysteroid, 65, 237
indications, 182
local, 62

significance in diagnosis, 213
weakness after, 63
Convolutions, 7
arteries of, 38
motor, 10
symptoms of disease, 171
Corpora geniculata, disease of, 174

quadrigemina, 175
Corpus striatum, 35 "

INDEX.

241

Corpus striatum, connection with cere-
bellum, 34

symptoms of disease of, 173
Cortex cerebri, 8

motor region of, 10
disease of, 171

structure of, 8
Cranial nerves (see Nerves, cranial)
Crossed amblyopia, 22, 69
Crossway, sensory, 16
Cms cerebri, fibres in, 12

lesions of, 169, 175

Deafness, 95

bilateral, 97
Decussation of optic nerves, 18

pyramids, 50
Degeneration, secondary, 3
Degenerative diseases, 231
Deglutition, impairment of, 98

in bulbar palsy, 107
Delirium, 115

expansive, 233

with headache, 117
Dentate nucleus, 37
Deviation of eyes, conjugate, 53

primary, 82

secondary, 82
Diagnosis of nature of lesion, 202

seat of lesion, 167
Diffuse functions, 45

symptoms, 49
Diplegia, 59
Diplopia, 83
Direct symptoms, 48
Discharge, 46

Disseminated sclerosis (see Sclerosis)
Double vision, 83

Ear, disease of, causing abscess of
brain, 200

causing deafness, 95
loss of taste, 25
pumlent meningitis, 224
Electrical irritability in hemiplegia, 56
facial paralysis, 92
hysterical hemiplegia, 236
Embolism, 191

Embolism, retinal, with cerebral, 211
Emotion, expression of, 122
Epilepsy after infantile hemiplegia, 194
Epileptic coma, diagnosis from apo-
plexy, 113
Exciting causes of convulsions, 64

vomiting, 152
Eye, changes in fundus, 158
Eye muscles —

external, centres for, 31

derangement in hysteria, 236
paralysis of, 82
internal, centres for, 31
paralysis of, 89
Eyes, associated movements, 88
conjugate deviation, 53, 88

Face, paralysis of, 91

in hemiplegia, 50, 58
Facial nerve, origin, 28

' paralysis, 91
Fibres, nerve, and nerve-cells, 4
posterior horizontal, 30
tortuous course of, 6
Field of vision (see Vision)
Fifth nerve —
motor part,
nucleus, 29
paralysis of, 90
sensory part,
nuclei, 29
paralysis of, 90
relation to taste, 25, 90
Focal symptoms, 48
Forced movements, 66
Fourth nerves, 30

paralysis of, 87, 88
Frontal lobe,

connection with cerebellum, 32
symptoms of lesion, 171
Fronto-cerebellar fibres, 32
Functional and organic disease, dif-
ferential diagnosis, 233
Function, recovery of, 45
Fundus oculi (see Eye)

Gait, cerebellar, 36, 179
Ganglia, central, 35

R

242

INDEX.

Ganglia, symptoms of disease of, 173
Gasserian ganglion, 90
General paralysis of insane, 233

articulation in, 105

congestive attacks in, 155

symptoms of, 233
Gesture, expression by, 121
Glosso-pharyngeal nerve, origin, 28

paralysis, 98

Haemorrhage, cerebral, 187
symptoms, 222

meningeal, 190
during birth, 196

retinal, 159

ventricular, 221
Half-vision centre, 21
Headache, 140

association with optic neuritis, 142
delirium, 117

functional, 140

paroxysmal, 141
in children, 155

significance, 217
Head, pain in, 140

unpleasant sensations in, 144
Hearing, affection of, 95

central relations, 25

method of testing, 95
Heart disease, causing embolism, 192

significance, 207, 216
Hemiansesthesia, 67

case, from organic disease, 17

hysterical, 69
Hcmiopia, 20

causation, 73

examination for, 77
Heniiopia from disease of thalamus,
173

nasal, 73

temporal, 73

varieties, 79
Hemiplegia, 50

alternate, 58

choreoid movements after, 59

congenital, 195

distribution of palsy in, 51

hysterical, 235

Hemiplegia, infantile (see Infantile
hemiplegia)

lesion on same side, 50

relation to seat of disease, .180

spastic, 194

varieties, 58
Hemisphere, right, use in speech, 125
Heredity, neurotic, 216
Hydrocephalus from iiyury during

birth, 197
Hyper-pyrexia in disease of pons, 154
Hypochondriasis, cephalic sensations
in, 144

loss of memory in, 118
Hypoglossal nerve, 26

nucleus, 26

paralysis, 106
Hysteria, affection of sight in, 22, 69

aphonia in, 102

coma, 113, 234

contracture in, 235

diagnosis from organic disease, 234

hemiansesthesia in, 69, 236

hemiplegia in, 235

in cases of brain disease, 65

paralysis of larynx in,
abductor, 101, 237
adductor, 102, 237

stupor in, 235

tremor in, 236

vomiting in, 150
Hysteroid convulsions in organic dis-
ease, 65

Images, double, 83
Incoherence of idea, 118
Incontinence of urine, 158
Inco-ordination, 66

cerebellar, 179
Indirect symptoms, 48
Infantile hemiple^a, causes, 194

congenital, 195

hysteria after, 70

recovery of sensation in, 69
Inflammation of brain, 197

of membranes (see Meningitis)
Insula (see Island of Reil)
Insular sclerosis (see Sclerosis)

INDEX.

243

Internal capsule (see Capsule)
Iris, centre for, 29

(See also Pupil)
Irritation, 46

sensory, 70

paroxysmal, 71
Island of Reil, symptoms of disease, 173

Joints, effusions into, in hemiplegia, 57
Kidney disease (see Bright's disease)

Labio-glossal paralysis, 107

articulation in, 232
Labyrinth, disease of, 95
Language, sensory relations of, 124
I^arynx, nerve-supply, 99

paralysis of, 100
in hysteria, 237
Lead-poisoning, optic neuritis in, 163
Leg, affection in hemiplegia, 52

centre, 10
Lenticular loop, 35

nucleus, 35
Leucocythsemia a cause of haemorrhage,

212
Lips, origin of fibres for, 29
Localization, 167

Mastication, muscles of, paralysis of, 90

in hemiplegia, 51
Medulla oblongata, nerve nuclei in, 26

symptoms of disease, 178
Memory, loss of, 117

in hypochondriasis, 118
for words, 123
defect, 127
Meningitis, 198

acute, symptoms, 224

varieties, 198
chronic, alcoholic, 226
syphilitic, 199
symptoms, 226
Mental symptoms, 108

significance of, 218
weakness, 117
juvenile, 119

Migraine in children, 155

sensory disturbance in, 71

visual symptoms in, 81
Mobile spasm after hemiplegia, 60
Monoplegia, 59
Moral sense, defects of, 119
Motor convolutions, 10

palsy, 49

path, 12
Movement, inco-ordination of, 66
Movements, forced, 66
Muscles, nutrition in hemiplegia, 56

of eyeball, paralysis, 86

of larynx, action, 99
paralysis, 100
unilateral and bilateral, 52
Myotatic irritability in hemiplegia, 54

Nausea, 150

Neck, paralysis of, congenital, 197
from disease of spinal accessory,
104
Nerves, cranial, 18

affection in hemiplegia, 58
associated palsies of bulbar nerves,
106
eye nerves, 106
course at base, 31
relation to motor tract, 31
significance of palsy of, 182
(See also under the several nerves)
Neurasthenia, 144
Neuritis, optic (see Optic)
Nuclei of cranial nerves (see vmder the

special nerves)
Nutrition of muscles in hemiplegia, 56

of skin, 57
Nystagmus, 218, 232

Oblique muscles of eyeball, paralysis

of, 87
Occipital lobe, relation to vision, 21

symptoms of disease, 172
Ocular vertigo, 86, 149
Oculo-motor nerves, 82

(See also Eye muscles)

244

INPEX.

Olfactory nerve, 24

symptoms of derangement, 72
Olivary bodies, 37
Onset, modes of, significance, 206
Ophthalmia, neuro-paralytic, 90
Ophthalmoplegia, 89
Ophthalmoscope, importance of, 158
changes revealed by, 158
in disease of optic nerve, 73
Opium-poisoning, diagnosis of apoplexy

from, 115
Optic chiasma, 18
nerves, 18
affection of, 73
atrophy of, 165

its significance, 217
decussation of, 18
irritation-symptoms, 81
neuritis, 73, 169
and headache, 142
significance of, 217
thalamus, 35
symptoms of disease of, 173
Orbicularis oris, innervation of, 29

Palate, nerve-supply, 27, 103
paralysis, 103, 104
in facial palsy, 93
Paralysis, motor,. 49

(See also Hemiplegia, etc. )
Paraplegia, congenital spastic, 197
Paresis, 49
Parietal lobe, symptoms of disease,

172
Parturition, injury to brain during, 194
paralysis after (see Puerperal state)
Perimeter, 76
Pharynx, paralysis of, 98
Phonic laryngeal palsy, 102
Phthisis, thrombosis in, 193
Pneumogastric nerve, origin, 26

paralysis, 98
Pons, circulation in, 41

disease of, effect on temperature,
154
symptoms of, 176
Position, loss of sense of, 68

Post-convulsive weakness, 63
Post-hemiplegic chorea, 59
Prefrontal lobe, 8
Premonitory symptoms, significance of,

205
Ptosis, 88

in hemiplegia, 182

in hysteria, 236
Puerperal state, thrombosis in, 193
Pulse, 156
Pupil, centre for reflex action, 29

affections of, 89

in paralysis of third nerve, 88
Pyramidal tracts, 12
Pyramids, decussation of, 50
Pyrexia, absence in inflammation, 154
(See also Temperature)

Reaction of degeneration, 92
Reading in loss of speech, 137
Recovery from hemiplegia, 57
Rectus muscles, paralysis of, 86
Recurring utterances, 132
Reflex action in hemiplegia, 54
Resistance in nerve-centres, 46
Respiration, centre for, 28

Cheyne-Stokes, 110, 157

disturbance of, 156

in apoplexy, 110

in diseases of medulla, 178
Respiratory paralysis of larynx, 102
Retina, changes in brain disease, 158

function in the two halves of, 20

hsemorrhages in, 159
Retinitis, albuminuric, 159
Rigidity in hemiplegia, 54

Sclerosis, disseminated or insular, 232
Seat of lesion, diagnosis, 167

in relation to symptoms, 212
Sensation, disturbance of, 67

loss of, in disease of motor cortex,
68, 171
in hemiplegia, 68
in hysteria, 69, 236
path for, 15
recovery in infantile lesions, 69

INDEX.

245

Senses, special, anatomy of nerves, 18
symptoms of disturbance, 71
(See also Vision, Smell, etc.,
and under the several nerves)
Sensory cortex, 16
crossway, 16
irritation, 70
s3nnptoms, 67
Sight (see Vision)
Signs, expression by, 121
Singing in speech-defect, 126
Sixth nerve, liability to pressure, 31
nucleus of, 28 .
paralysis, 86
Smell, nerve of, central relations, 24
examination of, 72

(See also Olfactory nerve)
Softening of brain, necrotic, 191

simple chronic, 190
Spasm after hemiplegia, mobile, 60
rigid, 54
tonic, 66
Speech, affection of, 120
centres, 124
congenital loss of, 197
sensory relations of, 123
Special senses (see Senses)
Sphincters, affection of, 157
Spinal accessory nerve —
external part, 6
course, 6
paralysis, 104
internal part,
nucleus, 27
paralysis, 100
Status epilepticus, temperature in, 155
Strabismus, 83

in hysteria, 236
Stupor, 109
Sudden lesions, 204
Symptoms, mechanism of, 44

relation to locality, 169
Syphilitic disease of arteries, 192
causing thrombosis, 192
coexisting with atheroma, 191
softening from, symptoms, 191
growths, 199
meningitis, 199, 227

Tache c^r^brale, 156
Taste, nerves of, 25
Temperature in apoplexy, 111
brain disease, 154

depression of, 155
Temporal lobe, affection of smell in
disease of, 72

connection with cerebellum, 33

symptoms of disease, 172
Tendon reflexes (so-called),

in hemiplegia, 54
Testamentary capacity in aphasia, 139
Tetanoid spasm, 66, 180
Third nerve, nucleus, 29

paralysis of, 86, 88
Thrombosis, 191

in arteries, 191
sinuses, 192
veins, 193
in childhood, 194
symptoms, 194
Tinnitus aurium, 97
Tongue, paralysis of, 105

in hemiplegia, 50
Tonic spasm after hemiplegia, 66

in cerebellar disease, 180
Tremor after hemiplegia, 59

hysterical, 236

significance of, 219, 232
Trophic changes after hemiplegia, 57

in eyeball, 90
Tumours of brain, 199

indications of nature, 228

symptoms, 227
Tuning-fork, use of, 95

Uraemia, diagnosis from apoplexy, 114
Urine, changes in, 157

incontinence of, 158
from mental state, 119

retention of, 158
Utterances, recurring, 132

Vascular lesions, 204
Vaso-motor changes, 156

in hemiplegia, 57
Veins of the brain, 41

thrombosis in, 193

246

INDEX.

Venous circulation, peculiarities, 41
Verbal amnesia, 128, 134
Vertigo, 145
aural, 148
epileptic, 149
gastric, 149
ocular, 86, 148
vomiting with, 149
Vision, centres for, 21
higher, 24
colour, examination, 75

fields for, 77
examiination of, 75
field of, 18
examination of, 76
projection of, 84
path, 21

Vision, transient loss of, 81

Vocal cords, paralysis of, 100

Voice in expression, 122

Voluntary movements in hemiplegia, 53

speech, 122
Vomiting, 150

White substance of cerebmm, 8

symptoms of disease, 173
Will, power of making a, in loss of

speech, 139
Word-blindness, 137
deafness, 125
order of loss, 134
Writing power, loss of, 134
preservation of, 131

Pardon di- Sinia, Printers, PcUemoster Bow, and Wine Office Court, London, B.C.

BY THE SAME AUTHOR.

THE DIAGNOSIS OF DISEASES OF THE
SPINAL COED. Second Edition. 8vo. With
Dlnstrations. Price 48. Qd.

EPILEPSY AND OTHER CHRONIC CON-

VULSIYE DISEASES: THEIE CAUSES,
SYMPTOMS, AND TEEATMENT. 8vo. Price
lOs. 6d.

A MANUAL AND ATLAS OF MEDICAL
OPHTHALMOSCOPY. With Sixteen Coloured,
Autotype, and Lithographic Plates. 8vo. Price IBs.

PSEUDO - HYPERTROPHIC MUSCULAR
PAEALYSIS : a Clinical Lecture. With Dlustra-
tions. 8vo. Price 3«. 6d.

Shortly.

A MANUAL OF DISEASES OF THE
NEEVOUS SYSTEM. For Students and Practi-
tioners.

LONDON : J. & A. CHUECHILL.

Catalogue B] London, \\, New Burlington Street

May, 1885.

SE L ECTI O N

J. & A. CHURCHILL'S GENERAL CATALOGUE

ALL RECENT WORKS PUBLISHED BY THEM

ftHT Ar<D pClBNCE OF MEDICIKE

N.B.— As Hr as possible, this List is nrranged in the order in
which medical study Is usually pursued

J. 4 A. CHDRCHUL pnMisli for the following Institutions
api Public Bodies:—

ROYAL COLLEGE OF SURGEONS. i

CATALOGUES OF THE MUSEUM. '

Twemy separate Catalogues (List and Prices can be abtaineil at J. & A. Churchill).

GUY'S HOSPITAL.

REPORTS BY THE MEDICAL AND SURGICAL STAFF.
Vol. XXVL. Third Series (1883). 75. M.

LONDON HOSPITAL.

PHARMACOPCEIA OF THE HOSPITAL. 3s.

CLINICAL LECTURES AND REPORTS BY THE MEDICAL AND
SURGICAL .STAFF. Vols. I. lo IV, 7s. 6d. each.

ST. BARTHOLOMEW'S HOSPITAL.

CATALOGUE OF THE ANATOMICAL AND PATHOLOGICAL
MUSEUM. Vol. I.— Pathology. 155. Vol. IL— Teratology, Anatomy
and Physiology, Botany. 7s. (id.

ST. GEORGE'S HOSPrTAL.

REPORTS BY THE MEDICAL AND .SURGICAL STAFF. j

The last Volume (X.} was issued in 18S0. Price 7s. 6d. I

CATALOGUE OF THE PATHOLOGICAL MUSEUM. 153. I

.'iUPPLEMENTARV CATALOGUE {1882). js. '

ST. THOMAS'S HOSPITAL.

REPORTS BY THE MEDICAL AND SURGICAL STAFF.

Annually. Vol. XL, New Series (i88z). 7s. 6d. .

MIDDLESEX HOSPITAL. I

CATALOGUE OF THE PATHOLOGICAL MUSEUM, izs, I

ROYAL LONDON OPHTHALMIC HOSPITAL. *

REPORTS BY THE MEDICAL AND SURGICAL STAFF.
Occasionally. Vol. X., Part III. (August, 1882). js.

OPHTHALMOLOGICAL SOCIETY OF THE UNITED KINGDOM.

TRANSACTIONS.

Vol. II. {1881-3). I2S. 6d.

MEDICO-PSYCHOLOGICAL ASSOCIATION. j

JOURNAL OK MENTAL SCIENCE. |

Quarterly. 3s. 6d. each, or 14s. per annum. M

PHARMACEUTICAL SOCIETY OF GREAT BRITAIN. ^

PHARMACEUTICAL JOURNAL AND TRANSACTIONS.
Every Saturday. 4d. each, or 20s. per annum, post free.

BRITISH PHARMACEUTICAL CONFERENCE.

YE.A.R book: of PHARMACY.

in December. IDs.

BRITISH DENTAL ASSOCIATION.

JOURNAL OF THF: ASSOCIATION AND MONTHLY REVIEW '
OF DENTAL SURGERY.
^^_ On the IJlh of each Month, &i. eadi, it 7s. per annum, post free. J

J. & A. CHDRCHllL'S GENERAL CATALOCDE,

ALL RECENT WORKS PUBLISHED BY THEM ON THE
ART AND SCIENCE OF MEDICINE.

N.B.— J: ^ ^. Churekill's Disi^riptivt List of iVarki m Cheinisiiy, Materia MtdUa,

Pharatary, Botany, P/urtograJi/ty, Zoelegy, thi Microscept, and othir Braiuhes

ef Science, can he had on application.

Practical Anatomy :

A Manual of Dissections. By Christopher
Heath, Surgeon to University College
Hospital Sixth Edition. Revised by

RlCKMAN J, GODLBE, M.S. LoRd.,

F.R.C.S., Demonatialor of Anatomy in
University ColleECi and Assistant Sui^;eon.
to the Hospital. Crown Svo, with 24
Coloured Plates and 274 Engravings, 15s.

■Wilson's Anatomist's Vade-
Mecum. Tenth Edition. By George
BtlCHAHAN, Professor of Clinical Surgery
in the University of Glasgow; and Henkv
E. Clark, M.R-C.S., Lecturer on Ana-
tomy at the Glasgow Royal Infirmary
School of Medicine. Crown Svo, with
450 Engravings (including 2.6 Coloured
Plates), iSs.

Braune's Atlas of Topographi-
cal Anatomy, after Plane Sections of
Froien Bodies. Translated by Edward
BelijIHY, Surgeon to, and Lecturer on
Anatomy, &c., at. Charing Cross Hos-
pital. Large Imp. Svo, with 34 Photo-
lithwraphic Plates and 4J5 Woodcuts, 40s.

An Atlas of Human Anatomy.
By RiCKMAN J. Godlee, M.S.,
F.R.C.S., Assistant Surgeon andSenior-
Demonstrator of Anatomy, University
College Hospital. With 48 Imp. 4to
Plates (IIZ figares), and a volume of Ex-
planatory Text, Svo, ;£4 t4s. 6d.

Surgical Anatomy :

A series of Dissections, illustrating the

Principal Repons of the Human Body.

By Joseph Maclise. Second Edition.

52 folio Plates and Text. ^3 izs.
Medical Anatomy.

By Francis Sibson, M.D., F.R.C.P.,

F.R.S. Imp. folio, with 11 Coloured

Plates, 435.

Anatomy of the Joints of Man.
By Henry Morris, .Suigeon to, and
Lecturer on Anatomy and Practical Sur-
gery at, the Middlesex Hospital. Svo,
with 44 Lithographic Plates (several being
coloured) and 13 Wood Engravings, 165.

Manual of the Dissection of the
Human Body. By Luther Holden,
Consulting Suigeon to St. Bartholomew's
Hospital. Edited by John Langton.
F.R.C.S., Surgeon lo, and Lecturer on
Anatomy at, St. Bartholomew's Hos-
pital. Filih Edition. Svo, with 208
Engravings, zos.

By the same Author.

Human Osteology.

Sixth Edition, edited by the Author and
James Shuter, F.R.C.S., M.A., M.B.,
Assistant Surgeon to St. Bartholomew's
Hospital. Svo, with 61 Litht^raphic
Plates and Sg Engravings. 16s.

Landmarks, Medical and Surgi-
cal. Fourth Edition. Svo. [In the Press.
The Student's Guide to Surgical

Anatomy ; An Introduction 10 Opera-
live Surgery. By Edward Bellamy,
F.R.C.S. and Member of the Board of
Examiners. Third Edition. Fcap. Svo,
with Engravings. [In the Press.

The Student's Guide to Human

Osteology. By William Warwick
Wagstakfe, late Assistant Surgeon lo
St. Thomas's Hospital. Fcap. Svo, with
23 Plates and 66 Engravings, los. 6d.
The Anatomical Remembran-
cer ; or. Complete Pocket Anatomist.
Eighth Eriilion, jzmo, 3s. 6d.

J. ^ A. CHURCHILL'S RECENT WORKS.

Diagrams of the Nerves of the

Human Body, eshibiiing their Origin,
Divisions, am) Connections, wilh their
nistribution to the Vattous Regions of
the Cutaneous Surface, and to all the
Muscles. ByW, H. Flower, f!R.S.,
F.R,C.S. Third Edition, with 6 Plates.
Royal 4I0, I2S.

Atlas of Pathological Anatomy.
By Dr. Lancer EAux. Translated bf
W. .S. Greenfibld, M.D., Professor
of Pathology in the University of Edin-
burgh. Imp. 8*0, with 70 Coloured
Plates, ^5 ss.

A Manual of Pathological Ana-
tomy. By C. Handfikld Tone.':,
M.B., F.R.S., and E. H. .Sisveking,
M.D., F.R.C.P. Edited by J. F.
Paynb, M.D., F.R.C.P., Lecturer
on General Patholo^ at St. Thoiiuis's
Hospital. Second Edition. Crown Svo,
with 195 Engravings, 16s,

Lectures on Pathological Ana-
tomy. By S. WiLKS, M.D., F.R.S.,
and W. MoxoN, M.D., Physician to Guy's
Hospital. Seconii Edition. Svo. PIates,l8s.

Post-mortem Examinations :
A Description and Explanation of the
Method of Perfonning them, with especial
reference to Medico-Legal Practice. By
Prof. ViRCHOW. Translated by Dr. T.
P. Smith. Second Edition. Fcap. Svo,
wilh 4 Plates, 35. 6d.

The Human Brain :

Histolt^cal and Coarse Methods of Re-
search. A Manital for Students and
Asylum Medical Officers. By W. Bevan
Lewis, L.R.C.P. Lond., Deputy Medi-
cal Superintendent to the West Riding
Lunatic Asylum. Svo, with Wood En-
gravings and Photographs, Ss.

Manual of Physiology :

For the use of Junior Students of Medi-
cine. By GERAi.n F. Yeo, M.D.,
F.R.C.S., Professor of Physiology in
King's College, London. Crown Svo,
with 300 Engravings, 145.

Principles of Human Physi-
ology. By W. B. Carpenter, C.B.,
M.D., F.R.S. Ninth Edition. By
Henry PtjwER, M,B., F.R.C.S. Svo,
with 3 Steel Plates and 377 Wood Engrav-
ings, 31s. 6<l.

Syllabus of a Course of Lectures
00 Physiology. By Philip H. Pve-
Smith, B.A., M.D,,F,R.C.P,, Physician
to Guy's Hospital. Crown Svo, with
Diagrams and an Appendix of Notes and
Tables, Ss-

Sanderson's Handbook for the
Physiological Laboratory. By E.
Kleik, M.D.. F.R.S. ; J. Burdon-
Sandbrson, M.D., F.R.S. ; Michael
Foster, M.D,, F.R.S. ; and T. Lauder
Brvnton, Af.D., F.R.S. 8vo, with 113
Plates, 24.?.

A Treatise on Human Physi-
ology. By John C. Dai.ton, M.D.
Seventh Edition. Svo, with 252 Engrav-
ings, 20s.

Histology and Histo- Chemistry
of Man. By Heineich Frev, Pro-
fessor of Medicine in Zurich. Translated
by Arthur E. J. Barker, Assistant
.Surgeon to University College Hospital.
Svo, with 608 Engravings, 21s.

The Law of Sex.

By G. B. Starkweather, F.R.G.S.
With 40 Illustrative Portraits. Svo, l6s.

Manual of the Laws Affecting
Medical Men. By Rout. G. Glenn,
LL.B., Barrister -a! -Law. WithaChapler
on Medical Etiquette, l^ A. Carpenter,
M.D. Svo, 14s.

Medical Jurisprudence :

Its Principles and Practice. By ALntBD
S. Tavlor, M.D„ F.R.C.P., F.R.S.
Third Edition, by Thomas Stbvbnsok,
M.D., F.R.C.P., Lecturer on Medical
JurLsprudence at Guy's Hosfnlal. 3 vols.
Svo, with iSS Engravings, 31s. 6d.
By the saait Aulhar.

A Manual of Medical Jurispru-
dence. Tenth Edition. Crown Svo,
with 55 Engravings, (4s.

Poisons, -^^J"-

In Relation to Medical Jurisprudence and
Medicine. Third Edition. Crown Svo,
with 104 Engravings, l6s.

Lectures on Medical Jurispru-
deni^e. By Francis Ocston, M.D.,
late Professor in the University of Aber-
deen. Edited by Francis Ogston, Jun.,
M.D. Svo, wilh la Copper Plates, 18s.

A Handy Book of Forensic
Meiiicine and Toxicology. By C,
Meymott Tidv, M.D., F.C.S., and W.
Bathurst WoonuAN, M.D., F.R.C.P.
Svo, with 8 Lithccraphic Plates and 116
Engravings, 31s. 6d.

The Student's Guide to Medical

Jurisprudence. By John Aber-
CROMHIE, M.D., Senior Assistant Physi-
cian to Charing Cross Hospital. Fcap. Svo,
7S. 6d.

Microscopical Examination of
Drinking "Water and of Atr. By
J. D. Macdonald, M.D., F.R.S., Ex-
Professor of Naval Hygiene in the Army
Medical School. Second Edition. Svo,
with 25 Plates, 7s. 6d.

Sanitary Examinations

Of Water, Air, and Food. A Vade-
Mccum for the Medical Officer of Health.
By Cornelius B. Fox, M.D., F.R.C.P.
Crown Svo, with 94 Engravings, 12s. 6d.
Dress: Its Sanitary Aspect.
A Paper read before the Brighton Social

Roth,' I

.A Manual of Practical Hygiene.

By K. A. I'ARKES, M.D., F.K.S. Sixth
Edition, by F. De Chaumont, M.D.,
F.R.S., Professor of Military Hroiene in
the Army Medical School. Bvo, with
Qiunermis Fktes and Engravings. iSs.

A Handbook of Hygiene and
Sanitary Science. By Geo. Wilson,
M.A., M.D., F.R.S.E., Medical Officer
of Health for Mid-Warwickshire. Fifth
Edition, Crown Svo, with Engravings,
los. 6d.

By Ihe sai/ie Aulhor.

Healthy Life and Healthy

Dwellings : A Guide to Personal and
Domestic Hygiene. Fcap. Svo, ss.
How to Arrest Infectious Dis-
eases, By Edgar G. Bar.nes, M.D.
Lond., Medical Officer of Health of the
Eye Urban ajid Hartismere Rural Ussii-
tary Districts. Fi^p. Svo, 2S. 6d.

Dangers to Health :

A Pictorial Guide to Domestic Sanitary
Defects. By T. PRIDCIN Teale, M.A.,
Sui^eon to ihe Leeds General Infirmary.
Fourth Edition, Svo, with 70 Lithograph
Plates {mostly coloured), los.

Hospitals, Infirmaries, and Dis-
pensaries : Their Construction, Inte-
rior Arrangemml, and Management;
with Descriptions of existing Institutions,
and 74 Illustrations. By F. Oppbrt,
M.D., M.R.C.P.L. Second Edition.
Royal Svo, 12s.

pay Hospitals and Paying

■Wards throughout the ■World.

By Henry C. Burdett, late Secretary to

the Seamen's Hospital Society. Svo, 7s.

By the same Aalhsr.

Cottage Hospitals — General,
Fever, and Convalescent ; Their
Progress, Management, and Work. Second
Edition, with many Flans and Illustra-

Hospital Construction and
lUanagement. By F, J. Mouat,
M.D., Local Government B<Kird Inspec-
tor, and H. Saxon Snell, Fell. Roy.
lost. Brit. ArchitecU, In 3 Parts, 4to,
15G. each; 01, the whole work bound in
half calf, with large Map, 54 Lithographic
Plates, and 27 Woodcuts, 35s.

Manual of Anthropometry :

A Guide to the Measurement of the
Human Body, containing an Anlhropo-
metrical Chart and Register, a Systematic
Table of Measuremt^ls, &c. By Charles
ROBRRTS, F.R.C.S. 8vo, with numerous
Illustrations and Tables, Ss. 6d.
By lie same Author.

Detection of Colour-Blindness
and Imperfect Eyesight. Svo, with

a Table of Coloured Wools, and iibeet of
Test-types, 5s. *■!•■-«..

A Manual of Psychological

Medicine. With an Appendix of
Cases. By John C. Buck.nill, M.D.,
F.R..S., and D. Hack Tukb, M.D.,
F,R.C.P. Fourth Edition. Svo, with I z
Plates (30 Figures) and Engravings, ajs.
Illustrations of the Influence of
the Mind upon the Body in
Health and Disease ; Designed to
elucidate the Action of the Imagination.
By Daniel Hack Ti;ke, M.D.,
F.K.C.P., LL.D. Second Edition,
z vols, crown Svo, 15s,

By the same Auikoi:

Sleep 'V^alking and Hypnotism.

AManualof Psychological Medi-
cine and Allied Nervous Dis-
orders. By Edward C. Mann, M.D.,

Memlier of the New York Medico-Legal
Society. With Plates. Svo, 24s.
Mental Diseases.

Clinical Lectures. By T. S. Clouston,
M.D., F.R.C.P. Edin., Lecturer on
Mental Diseases in the University of
Edinburgh. With 8 Plates (6 Coloured).
Crown Svo, 12s. 6d.

The Student's Guide to the
Practice of Midwifery. ^ D.
Li/)YD Roberts, M.D., F.R.C.P., Lec-
turer on Clinical Midwifery and Diseases
of Women at Owen's College; Physician
to St. Mary's Hospital, Manchester. Third
Edition. Fcap. Svo, with 2 Coloured
Plates and 127 Wood Engravings, 7s. 6d.

Handbook of Midwifery for Mid-
wives: By J. E. EuRTO.li, L.R.C.P.
Lond., Surgeon to the Hospital for
Women, Liverpool. Second Edition.
With Engravings. Fcap. Svo, 6s.

Lectures on Obstetric Opera-
tions i Including the Treatment of
Haemorrhage, and forming a Guide to
the Management of Difficult Labour.
By Robert Barnes, M.D., F.R.C.P.,
Obstetric Physician to Si. Ceoige's Hos-
pital. Third Edition. Svo, with 124
Engravings, iSs.

By the saiae Author.

A Clinical History of Medical
and Surgical Diseases of

"Women. -Second Edition. Svo, with
iSl Engravings, 2Ss.

Clinical Lectures on Diseases
of ■Women ; Delivered in St. Bartho-
lomew's Hospital, by J. Matthews
Duncan, M.D., F.R.C.P., F.R.S.E.
Second Edition. Svo, 14s.
By the saint Atitksr.

Sterility in Woman.

Being the Gulstonian Lectures, delivered
in the Royal Colt^e of FhyikiAna, in
Feb., 1S83. Svo, 63.

J. vS" A. CHURCHILL'S RECENT WORKS,

The Student's Guide to the
Diseases of 'Woinen, By Alfreo
L. Galahfn, M,D., F.R.C.P., Obstetric
Physician to Uuy's Hospital. Third Edi-
tion. Fcai],8vo,wilh78Engraviiigs,7s.6d.

West on the Diseases of
Women. Fourth EJitbn, revised by
the Author, with numerous Additions ^
J.MatthewsDun-can.M.D., F.R.C.P,,
F.R.S.E., Obstetric Physician to St. Bat-

Iholoii

■s Ho

ipital.

Fcap.

Notes on Diseases of Women :

Specially designed to assist the Student
in preparing tor Examination. By J. J.
Rb¥NOlds,L.R.C,P.,M,R.C.S. Second
Edition. Fcap. 8vo, 2s. 6d.
By the same Author.
Notes on Midwifery :

Specially designed for .Students preparing
for Examination. Fcap. Svo, 4.1.
Dysmenorrhcea, its Pathology
and Treatment. By Hey wood Smith,

M.D. Oxon., Physician lo the Hospital
for Women, &c. Crown 8vo, with En-
graving 4s. 6d.

Obstetric Aphorisms :

For the Use of Students commencinp
Midwifery Practice. By J
SwAVNE, M.D. Eighth Edit
8vo, with Engravings, 3s. 6d.

Obstetric Medicine and Surgery :
Their Principles and Practice. By F. H.
Kamshotham, M.D., F.R.C.I'. Fifth
Edition. 8vo, with 120 Plates, zzs.

Schroeder's Manual of Mid-
wifery, inetudingthe Pathologyof Preg-
nancy and the Puerperal .Slate. Trans-
lated by Charles H. CAKTEk, B.A,
M.D. Svo, with Engravings, tzs. 6d.

Influence of Posture on ^Vomen
in Gynccic and Obstetric Practice. By
J. H. AvELiNG, M.D., Physician lo the
Chrfsea Hospital for Women. 8vo, 6s.
By the same Author.

The Chamberlens and the Mid-
ivlfery Forceps; Memorials of the
Family, and an Essay on the Invention of
the Instnimenl. 8vo, with Engravings,
7s. 6d.

A Handbook of Uterine Thera-
peutics, and of Diseases of Women.

By E. J. Tilt, M.D., M.R.C.P. Fourth
Edition. Post 8v-o, los.

By the same AiUhor.
The Change of Life

In Health and Disease : A Clinical
Treatise on the Diseases of the Nervous
System incidental to Women at the De-
clineofLife. Fourth Edition. Svo, los. 6d.
Chronic Disease of the Heart :
Its Bearings upmn Pr^nancy, Parturition,
and Childbed. By Angus Macdonald,
M.D., F.R.S.E., Physician to the Edin-
hurgh Royal Infirmary. Svo, with En-
gmvings, 8s. 6d.

Ovarian and Uterine Tumours:

Their Pathology and Surgical Treatment.
By Sir T. Spencer Wells, Bart.,
F.R.C.S., Consulting Surgeon to the
Samaritan Hospital, 8vo, with En-
gravings, 2IS.

By the same Author.
Abdominal Tumours:

The Principles and Practice of
Gynaecology. By Thomas Addis <
Emmet, M.D., Surgeon to the Woman's
Hospital, New York. Third Edition,

and Fallopian Tubes : A Practical

Treatise by A. Courtv, Prafessor of
Clinical Surgery, Montpellier. Translated
from Third Edition by his Ihipi), Agnes
McLaren, M.D., M.K.Q.C.P.I., with
Preface by J. Matthews Duncan, M.D.,
F.R.C.P. Svo, with424EngravinKi, 24s.

Backward Displacements oT the
uterus and Prolapsus Uteri ;
Treatment by the New Method of Short-
ening the Round Ligaments. By Wil-
liam Alexander, M.D., M.Ch.Q.U.l.,
F.R.C.S., Su^eon to the Liverpool Infir-
mary. Crown8vo,with Engravings,3s.6d.

The Female Pelvic Organs:

Plafes taken from Nature % with Com- ,
menlaries. Notes, and Cases. By Hknky I
Savage, M.D., F.R.C.S., Consultir^ ]
Officer of the Samaritan Free HospltaL \
Fifth Edition, Roy. 410, with 17 Litho-
graphic Plates(rs colouredjand 5a Wood- '
cuts, {,1 15s.

The Student's Guide to Diseases <
ot Children. By Jas. F. Goodkart,
M.D., F.R.CP., Assistant Physician to
Guy's Hospital ; Physician to the Evelina ^
Hospital (or Sick Children. Fcap. Svo, I
los. 6d. ,

The Wasting Diseases of Infants
and Children. By EtisTACE Smith,
M.D., Physician to the King of the I
Belgians, Physician lo the East London 1
Hospital for Children. Fourth Edition. 1
Post Svo, 85, fid.

A Practical Treatise. Svo, ais.

AtSB.

Clinical Studies of Disease in

Children. Second Edition, Post Svo.
[/n the Press.

A Practical Manual of the

Diseases of Children. With a For-
mulary. By Edward Ellis, M.D,

Fourth Edition. Crown 8vo, IDs.
By the same Author.

^Manual of what every Mother

sUOAxVd VmO'w . Fca\i. Svo, is. 6d.

3. ^ A. CHURCHILL'S RECENT WORKS.

A Treatise on the Diseases of

Children. For Practitioners and
Students. By W. II. Day, M.D., Physi-
cian to the Samaritan Hoscital. Second
Edition. Crown Svo. \ln Ihe Priss.

Infant Feeding and its Influ-
ence on Life ; By C. H. F. Routh,
M. D. , Physician lo the Samatilan Hospital
Third Edition. Fcap. 8vo, 7s. 6[i.

A Manual for Hospital Nurses

and others engaged in Attending on the
Sick. By Ehward J, Domville,
Surgeon 10 the Exetet Lying-in Charity.
Fifth Edition. Crown Svo, zs. 6d.

A Manual of Nursing, Medical
and Surgical. By Charles J. Cul-
LINGWOkTH.M.D., Physician toSt. Mary's
Hospital, Manchester. Second Edition.
Fcap. Svo, with Engravings, 33. 6d.
By Ihe same Aiitlim:

A Short Manual for Monthly

Nurses. Fcap. Svo, is. fid.

Notes on Fever Nursing.

ByJ. W. Au-AN, M.B., .Superintendent
and Physician, Glasgow Fever Hospital.
Crown Svo, with Engravings, zs. fid.

Manual of Botany:

Including the Structure, Functions, Clas-
sification, Properties, and Uses of Plants.
By Robert Bentlev, Professor of' Bo-
tany in King's College and to the Phar-
nuLceulical Society. Fourth Edition.
Crown Svo, with i.lS; Engravings, 15s.
By Hit same Author.

The Student's Guide to Struc-
tural, Morphological, and Phy-
siological Botany. With fifio En-
gravings. Fcap. Svo, 7s. fid.

AtsD.

The Student's Guide to Syste-
niatic Botany, including the Classi-
fication of Plants and Descriptive Botany.
Fcap. Svo, with 350 Engravings, 3s. fid.

Medicinal Plants :

Being descriptions, with original figures,
of the Principal Plants employ^ in
Medicine, and an account of their Pro-
perties and Uses. By Prof- Bkntley and
Dr. H, Thimen. In 4 vols., large 8vo,
with 306 Coloured Plates, bound in Half
Morocco, Gilt Edges, jftl lis.

Therapeutical Remembrancer.
ByJOHNMAVNE, M.D. Second Edition,
ifimo, 3s. 6d.

By the saaie Anther,

Notes on Poisons.

Mounted and Varnished, i8byi2in., is.M-

The National Dispensatory :

Containing the Natural H istory. Chemistry,
Pharmacy, Actions and Usesof Medicines.
By Alfred Still6, M.D., LL.D., and
• iiNM.MAisCK,Ph-D. Third Edition.
}i,3^tL41l Engravings, 365.

Royle's Manual of Materia

Medica and Therapeulica. Sinth
Edition. By John Harley, M.D.,
Physician to St. Thomas's

Crowi

, ISS.

The Student's Guide to Materia
Medica and Therapeutics. By
John C. Thorowgood, M.D., F.R.C.P.

Second Edition. Fcap. Svo, 7s.

Materia Medica and Therapeu-
tics. By Charles D. F. Phillips,
M.D., F.K.S. Edin., late Lecturer on
Materia Medica and Therapeutics at the
Westminster Hospital Medical School.

Vol. 1 — V^etahle Kingdom. Svo, 153.

Vol. 3 — Inorganic Substances. Svo, 21s.

Binz's Elements of Thera-
peutics: A Clinical Guide to the Action
of Drugs. Translated by E. I, SPARKS,
M.B., F.R.C.P. Crown Svo, Ss. fid.

Materia Medica.

A Manual for the use of Students. By
ISAMBARD Owen, M.D., Lecturer on
Materia Medica, &c., to St. George's
Hospital. Crown Svo, 6s.

The Pharmacopoeia of the Lon-
don Hospital. Compiled under the
direction of a Committee appointetl by the
Hospital Medical Council. Fcap. Svo, 3s.

A Companion to the' British

Pharmacopoeia. By Peter Squire,

F.L.S., assisted by his Sons, P. W. and

A. H. Squire. 13th Edition. Svo, ios.6d.

By the same Anthers,

The Pharmacopceias of the Lon-
don Hospitals, arranged in Croups
for Easy Reference and Comparison.
Fifth Edition. iSmo, 6s.

Bazaar Medicines of India,

And Common Medical Plants : With FuQ
Index of Diseases, indicating Iheir Treat-
ment by these and other Agents procur-
able throughout Iniiia, S:c. By E. J.
Waring, C.I.E.,M.D.,F.R.C.P. Fourth
Edition. Fcap. Svo, 5s.

Tropical Dysentery and Chronic
Diarrhoea — Liver Abscess ^ Malarial
Cachexia— Insolation — with other forms
of Tropical Diseases, &c. By Sir Joseph
Kayekr, K.C.S.I., M.D. Svo, iss.
Sy the sanif Author.

Climate and Fevers of India,

with a series of Cases (Croonian Lec-
tures, tSS2). Svo, with 17 Temperatuie
Charts, izs.
Family Medicine for India.

A Manual. By William J.MooRE,M.D.,
C- 1. E. , Honorary Sui|;eon to the Viceroy
of India. Published under Ihe Authority of
the Government of India. Fourth Editiott.
Post Svo, with 64 Engravings, IM.
By the same Author.

Health- Resorts for Tropical
Invalids, in India, at Home, and
Abroad, Post Svo, 5s. ^^^^

J. ^ A. CHURCHILL'S RECENT WORKS.

Spirillum Fever

(Synonyms, Famine or Relapsing Fever),
ax seen in Western Indii. By H. Van-
DVKB Carter, M.D., Su^eon-Major
I.M.D. Svo, with Plates, 21s.
Diseases of Tropical Climates,
And Iheir Treatment : With Hints for ihi;
Preservation of Health in the Tropics,
By James A. Horton, M.D., Suigeon
Major. Second Edition. Post Svo, iZ5.6d.

The Student's Guide to the
Practice of Medicine. By Mat-
thew Charteris, M.D., Professor of
Materia Medica in the University of
Glasgow. Third Edition. Fcap. Svo,
with Engravings on Copper and Wood, 7s.

Hooper's Physicians' Vade-
Mecum. A Manual of the Principles
and Practice of Physic, Tenth Edition.
By W. A. Guv, F.R.C.P.. F.R.S., and
J. IlAHLEY, M.D., F.R.C.P. With 118
Engravings. Fcap. Svo, izs. 6d.

Clinical Medicine :

Lectures and Essays. By Balthazar
Foster, M.D., F.R.C.P. Lond., Pro-
fessor of Medicine in Queen's College,
Birmin^am. Svo, IDs. 6d.
Clinical Medicine :

A Systematic Treatise on the Diagnosis
and Treatment of Disease. By Austin
Flint, M.D., Professor of Medicine in
the Betlevue Hospital Medical College.

By the same Authar.

Phthisis :

In a series of Clinical Studies. Svo, i6s.

The Student's Guide to Clinical

Medicine aad Case-Taking. By

Francis Warner, M.D., F.R.C.P.,
Asaslani Physician to the London Hos-
pital. Second edition. Fcap. Svo, 5s.
The Student's Guide to Medical
Diagnosis. By Samuel Fenwick,
M.D., F.R.C.P., Physician to the Lon-
don Hospital. Fifth Edition. Fcap.
Svo, with tii Engravings, 7s.
By the samt Author.

The Student's Outlines of Medi-
cal Treatment. Second Edition.

AhB.
On Chronic Atrophy of the

.Stomach, and on the Nervous Affections
of the Digestive Oigans. Svo, Ss.
How to Examine the Chest :
Being a Practical Guide for the use of
Students. By Samuel West, M.D.,
Physician 10 the City of London Hospital
for EHseases of the Chest ; Medical Tutor
and Registrar at St. Bartholomew's
Hospital. With 4a Engravings. Fcap.
Svo, js.

The Microscope in Medicine.

By Lionel S. Beale, M.B., F.R.S.,
Phy.sician lo King's ColWe Hospital,
Fourth Edition. Svo, with S Plates, 21s.

The Spectroscope in Medicine.

By Charles A. MacMunn, B.A., M.D.
Svo, with 3 Chromo- lithographic Plates of
Phyi^ological and Pathological Spectra,
and 13 Engravings, gs.

The Contagiousness of Pulmo-
nary Consumption, and its Anti-
septic Treatment. By J. Burnev
Vco, M.D., Physician lo King's Coil^e
Hospital. Crown Svo, 31. 6d.

Diseases of the Chest :

Contributions lo their Clinical History,
Palhol<^, and Treatment. By A. T.
Houghton Waters, M.D., Fhyudan
lo the Liverpool Royal Infiimaiy,
Second Edition. Svo, with Plates, ite.

The Operative Treatment of In- ■
tra-thoraclc KHusloa. Fothergiltiu

Assistant House- Surgeon, General In-
firmary, Leeds ; and Senior House-Sur-
geon, Inlirmaiy, Hudderslield. Witb
Engravings. Crown Svo, 6s.

Winter Cough

(Catarrh, Bronchitis, Emphysema, Asth-
ma). By Horace Dobkll, M.D.,
Consulting Physician lo the Royal Ho>-
pital for Diseases of the Chest. Third Edi-
tion. Svo, with Coloured Plates, ■as.6d.
By the same Author.

Loss of Weight, Blood- Spitting,
and L.ung Disease. Second Edition,
to which is added Part VI., " On the
Functions and Diseases of the Liver."
Svo, with Chromo-lithcgraph, los. fid.
Alsc.

The Mont Dore Cure, and the
Proper Way to Use it. Svo, 7s. M.

Notes on Asthma :

Its Forms and Treatment. By John C.
Thokowgooi), M.D., Phydcian to the
for Diseases of the Chest. Thir^

Editi

n Svo, 4S. 6d.

Croonian Lectures on Some
Points in the Pathology and
Treatment of Typhoid Fever,
By William Cayley, M.D., F.R.C.P.,
Physician to tlieMiddlesex and (he London
Fever Hosoitals. Crown Svo, 4s. fid.

Diseases of the Heart and Aorta :
Clinical Lectures. By G. W. Balfodr,
M.D., F.R.C.P., F.R.S. Edin., late
Senior Physician and Lecturer on Clinical
Medicine, Royal Infirmary, EdinbUKh.
Second Edition. Svo, with Chromo-litho-
graph and Wood Eogr»vings, lis. fid.

Manual of the Physical Dia-
gnosis of Diseases o( the Heart,
including ihe use of the Sphygmograph
and Catdiograph. By A. E. SanSOM,
M.D., F,R.C.P., Assistnnt Physician to
Ihe Lonilon Hospilal. Third Edition.
Fcap. 8vD, with 48 Engravings, 7s. 6d.

Idedical Ophthalmoscopy :

A Manual and Alias. By WiLLIAM R,
GowFKS, M.D., F.R.C.P., Assistant
Piofessor 0/ Clinical Medicine in Univer-
sity College, and Senior Assistant Phy-
sician Id the Hospital. Second Edition,
with Coloured Autotype and Lithc^raphic
Plates and Woodcuts. Svo, 18s.
Sy the same Author.

£pilepsy, and other Chronic

Convulsive Diseases ; Their Causes,
Symptoms, and Treatment. Svo, los. 6d.
Aho.

Pseudo-Hypertrophic Musctilar

Paralysis : A Clinical Lecture. Svo,

with Engravings and Plate, 3s. 6d.

Abs.

The Diagnosis of Diseases of

the Spinal Cord. Third Edition.

Svo, with Engravings, 4s. 6d.
Studies on Functional Nervous

Disorders. By C. Handfield Jones,

M.B., F.R.S., Physician to St. Mary's
Hospital. Second Edition. Svo, iSs.

(Visceral Neuroses :

Seine the Gulstonian Lectures on Neural-
gia of the Stomach, and Allied Disorders.
By T. Clifford Allbutt, M.A., M.D.
Canlab., F.R.S.. F.R.C.P., Consulting
Phy^cian to the Leeds General Infirmary.
Svo, 4s. 6d.

Diseases of the Nervous System,
Lectures delivered at Guy's Hospital. By
Samuel WiLKS, M.D., F.R.S. Second
Edition. Svo, iSs.
Nervous Diseases:

Their Description and Treatment. A
Manual for Students and Practitioners of
Medidne. By Allen M. Hamilton,
M.D., Phyacian at the Epileptic and Para-
lytic Hospital, New York. Second Edi.
tion. Royal Svo, with 72 Engravings, 16s.

■Diseases of the Nervous System:

Especially in Women. By S. Weir
MlTCKELL,M.D., Physician to the Phila-
delphia Infirmary for Diseases of the
Nervous System. Second Edition. Svo,
with < plates, 8s.

Nerve Vibration and Excitation,
aa Agents in the Treatment of
Functional Disorder and Organic
Disease. By J. Mortimer Granville,
M.D, Svo, js.

Notes on Rheumatism.

By Julius Pollock, M.D., F.R.C.P.,
Senior Physician Co Ihe Chaiing Cross
Hospital. Second Edition. Fcap. Svo,
with Engravings, 3s. 6d.

Diseases of the Liver:

With and without Jaundice. By George
Hablev, M.D., F.R.C.P., F.R.S. Svo,
with 2 Plates and 36 Engravings, ais.
Diseases of the Stomach:

The Varieties of Dyspepsia, their
Diagnosis and Treatment. By S. O.
Habershon, M.D., F.R.C.P. Third
Edition. Crown Svo, 5s.

By l/is same Author.

Pathology of the Pneumo-

gastric Nerve : Being the Lumleian
Lectures for 1876. Post Svo, 3s. 6d.
Also.

Diseases of the Abdomen,

Comprising those of the Stomach and other
parts of the Alimentary Canal, (Esopha-
gus, Crecum, Intestines, and Peritoneum.
Third Edition. Svo, with 5 Plates, 21s.
Acute Intestinal Strangulation,

And Chronic Intestinal Obstruction(Mode
of Death from). By Thomas Bkyant,
F.R.C.S., Senior Surgeon to Guy's
Hospital. Svo, 33.
Gout, Rheumatism,

And the Allied Affections ; with Chapters
on Longeviq' and Sleep. By Peter
Hood, M.D. Third Edition. Crown
Svo, 7s. 6d.

Diseases of the Nervous System.
Clinical Lectures, By Thomas Buzzard,
M.D., F.R.C.P., Physician to theNalional
Hospital for the Paralysed and Epileptic.
With Engravings, Svo. 15s.

A Treatise on the Diseases of
the Nervous System. By James
Ross, M.D., F.R.C.P., Assistant Physi-
cian to the Manchester Royal Infirmary,
.Second Edition. 2 vols. Svo, with Litho-
graphs, Photographs, and 332 Woodcuts,
5JS. 6d.

Fits :

Diagnosis and Immediate Treatment of
Casesoflnsensibilityand Convulsions. By
John H. Waters, M.D., K.C.Sl.G.C,
Surgeon to the C Division of Metropoli-
tan Police. Crown Svo, 4S.

Food and Dietetics,

Physiologically and Therapeutically Con-
sidered. ByF. W. Pav¥,M.D.,F.R.S.,
Physician to Guy's Hospital. .Second
Edition. Svo, 15s.

By the same Author.

Croonian Lectures on Certain

Points connected with Diabetes.

Svo, 4s. 61I.

Headaches :

Their Nature, Causes, and TreaEment.
By W. H. Day, M.D., Ph;ysician lo the
Samaritan Hospital. Third Edition.
Crown Svo, with Engravings, 6s. 6d.
On Megrim, Sick Headache, and
some Allied Disorders : A Contrihu-
tion to the Patholi^ of Nerve Storms. Bj
E, LivEiKG, M.D., F.R.C.P. Svt), Ifi^-

J. i- A. CHURCHILL'S RECENT WORKS.

Winter and Spring

On the Shores of Ihe Mediterranean. By
Hknkv Rennet, M.U. Kifth Ediiion.
Post Svo, with numerous Plates, Maps,
and Engravings, izs. 6d.

By llie same Author.

Treatment of Pulmonary Con-
sumption by Hygiene, Climate, and
Medicine. Third Edition. Svo, 7s. 6d.
Also.

Nutrition in Health and Disease.

Third (Library} Ediiion, Svo, 53, ; Cheap
Ediiion, fcap. Svo, 2s. 6d.
The Riviera :

Sketches o[ the Health- Resorts of the
Coast of France and Italy, from Hyeres to
Spezia : its Medical Aspect and Value, Sic.

By Edward I. Sparks, M.B., F.R.C.P.

Crown Svo, 8s. 6d.

The Principal Southern and
Siviss Health- Resoria : iheit Cli-
mate and Medical Aspect. By WlLllAM
Marcet.M.D., r.R.C.P.,F.R.S. With
lUuslialions. Crown Svo, 7s. 6d.

Medical Guide to the Mineral
■Waters of Fraiice and its Win-
tering Stations, With a Special
.Map. ByA. VlNTRAS, M.D., Physician
to the French Embassy, and to the French
Hospital, London. Crown Svo, Ss.

The Ocean as a Health-Resort :

A Practical Handbook of the Sea, for the
use of Tourists and Health- Seekers. By
Williams. WtLSON, L.R.C.P. Second
Edition, with Chart of Ocean Routes, &c.
Crown Svo, 73. 6d.

Principal Mealth-Resorts

Of Europe and Africa, and their Use in
the Treatment of Chronic Diseases. By
T. M. Madden, M.D. Svo, ios.

Handbook of Medical and Sur-
gical Electricity. By Herbert
TiHHlTS, M.D., F.R.C.P.E., Senior
Physician to the West London Hospital for
Paiaiy^s and Epilepsy. Second Edition.
Svo, with 95 Engravings, 9s.
By Ihe same Aulhor.

A Map of Ziemssen's Motor
Points of tiie Human Body : A
Guide to Localised Eleclrisation. Mounted
on Rollers, 35 x 21. With 20 Illustra-
tions, Ss.

Electricity and its Manner of
■Working in the Treatment of
Disease. By Wm, E. Steavenson,
M.D., Casually Physician and Electrician
to St. Bartholomew's Hospital. Svo,

Mechanical Exercise a Means
of Cure T Being a Description of the
Zander Institute, London ; its History,
AfipJj'anccs, Scope, and Object. Edited
by the Medical Officer of the Institution.
Crown Svo, wilh 24 Engravings, 2s. W.

Ambulance Handbook forVoIun-

teers and Others. By J. Akdavon
Rave, L.K. & Q.C.P.L, L.R.CS.I.,
late Surgeon to H.B.M. Transport No.
14, Zulu Campaign, and Surgeon E.I.R.
Rifles. Svo, with 16 Plates|50 figures),
3s. 6d.
A System of Practical Surgery.
BySirW.FEKCussoN,Bart..F.R.S. Fifth
Edition. Svo, with 463 Engravings, 21s.

Surgical Emergencies :

Together with the Emergencies Attendant
on Parturition and the Treatment of '
Poisoning. By Paul Swain, F.R.C.S.,
Surgeon to IheSouthDevonandEastCom- '
wall Hospital. Third Edition. Crown
Svo, with 117 Engravings, 5^-

Operative Surgery in the Cal-
cutta Medical College HospitaL

Statistics, Cases, and Comments. By <
Kexnetk McLeod, A.M., M.D,,
F.R.C.S.E., Surgeon -Major, Indiaa I
Medical Service, Professor of SurgOT
in Calcutta Medical College, Svo, with '
Illustrations, 12s. 6d.
A Course of Operative Surgery.
By Christopher Heath, Surgeon to
University College Hospital. Second |
Edition. Wilh 20 coloured Plates (iSo'
6guies) from Nature, by M. LEVeiLL^ |
and several Woodcuts. Large Svo, 3O8. j
By the same Author. I

The Student's Guide to Sui^ical \

Diagnosis. Second Ediiion. Fc^
Svo, 6s. 6d.

Also.
Manual of Minor Surgery and
Bandaging. For the use of House- |
Surgeons, Dressers, and Junior Practi- ,
tioners. Seventh Edition. Fcap. Svo, |
with 129 Engravings, 6s.

Injuries and Diseases of the ,
Jaws. Third Edition. Svo, wilh Plate
and 206 Wood Engravings, 14s.

Outlines of Surgery and Sun-
gical Pathology. By F. Le GRoa
Clark, F.R.S., assisted by W. W.
Wagstaffe, F.R.C.S. Second Edition.

Svo, I

L6d.

Surgical Enquiries :

Including the Hastings Essay on Shock, dw '
Treatment of Inflammations, andnumeroiu I
Clinical Lectures. ByF0RNEAUXjORDA»i.(
F.R.C.S., Professor of Surgery, Queen^i
College, Birmingham. Second E^tion,'
with numerous Plates. Royal Svo, izs.ed.
On Dislocations and Fractures.
By Joseph Maclise, F.R.C.S. Uni-
form with " Surgical Anatomy." 36 ftdio
?toei3.nd Texl. Cloth, ^a io«. ^. ^

J. ^ A. CHURCHILL'S RECENT WORKS.

The Practice of Surgery:

A Manual. By Thomas Bay ant,
Surgeon to Guy's Hospital. Fourth
Edition. 3 vols, crown 8vo, with
750 Engravings (many being coloured),
and inctud ing 6 chromo- lithographic plates,
3as.
The Surgeon's Vade-Mecum:

AManualofModernSurgery. ByRoHERT
Dbuitt, F.R.C.S. Eleventh Edition.
Fcap. 8vo, with 369 Engravings, 145.
Regional Surgery :

Including Surgical Diagnosis. A Manual
for the use of Students. By F. A.
SOUTHAM, M.A., M.B., F.R.C.S., As-
sistant Surgeon to the Manchester Royal
Infimiaty. Part I. The Head and Neck.
Crown 8vo, 6s. 6d. — Part II. The
Upper Extremity and Thorax. Crown

8vo,

!. 6d.

Illustrations of Clinical Surgery.

By Jonathan Hutchinson, F.R.S.,

Senior Surgeon to the London flospitah
In occasional fasciculi. I. to XVI., 6s. 6d.
each. Fasciculi !. to X. bound, with
Appendix and Index, ^3 ids.
By tlie same Author.

'jPedigree of Disease :

Being Six Lectures on Temperament,

Idiosyncrasy, and Diathesis. 8vo, js.

Treatment of Wounds and Frac-

' tures. Clinical I,eclures, By Sampson

' Gamgbb, F.R.S.E., Surgeon to the

Queen's Hospital, Birmingham. Second

Edition. iJvo, with 40 Engra.vings, los.

JTractures :

A Treatise. By Lewis A. Stimson,
B.A., M.D., Professor of Surgical Patho-
Iqgyin the University of New York. 8vo,
with 360 Engravings, jis.
Injuries of the Spine and Spinal
Cord, and NERVOUS SHOCK.

in their Surgical and Medico- Legal
Aspects, By Herheht W. Page, M.C.
Cantab., F.R.C.S., .Surgeon to St. Mary's
Hospital. Second Edition, post 8vo, los.
Lectures on Orthopaedic Sur-
gery. By Bernard E. Brouhurst,
F.R.C.S., Surgeon to Ihe Roj^al Ortho-
ptic Hospital. Second Edition. Svo,
with Engravings, 12s, 6d.

By the same Aiilhur.

On Anchylosis, and the Treat-
ment for the Removal of De-
formily and the Restoration of
Mobility In Various Joints.
Fourth tlilition. Svo, with Engravings, 55.
Also.

Curvatures and Diseases of the
Spine. Third Edilion. Svo, w ith
Engravings, 6s.

Hernia :

A Practical Treatise. By Joseph H.
Warren, M.D. Second Edition. Roy.
8vo, with Plates and S2 Engravings, 21s.
By Ike same Atilhsr.

A Plea for the Cure of Rupture ;
or, The Pathology of the Subcutaneous
Operation by Injection. 8vo, with Dia-
grams, 5s. 6d.

OrthopEedic Surgery,

And Diseases of the Joints. By L, A.
Savre, M.D., Professor of Orthopedic
Suraety in Bellevue Hospital Medical
College. Second Edition. Svo, with
Coloured Plate and 324 Engravings, ais.

Clubfoot :

Its Causes, Pathology, and Treatment.
By Wm. AliAMS, F.R.C.H., Surgeon to
the Great Northern Hospital. Second
Edition. 8vo, with io6 Engravings and
6 Lithographic Plates, 15s.

By Ihe same Aulhor.

On Contraction of the Fingers,

and its Treatment by Subcutaneous Opera-
tion ! and on Obliteration of Depressed
Cicatrices, by the same Methoii. Svo,
with 30 Engravings, 4s. 6d.
AhB.

Lateral and other Forma of
Cun^ature of the Spine : Their
Patholcgy and Treatment. Second Edi-
tion. Svo, with 5 Lithographic Plates and
72 Wood Engravings, los. fid.

Spinal Curvatures :

Treatment by Extension and Jacket ; with
Remarks on some Affections of the Hip,
Knee, and Ankle-joints. By H. Mac-
NAt;GHTON Jones, M.D., F.R.C.S.L

and Edin. Post Svo, with 63 Engravings,

On Diseases and Injuries of the

Eye i A Course of Systematic and
Clinical Lectures to Students and Medical
Practitioners. By J. R. WoLFE, M.D.,
F.R.C.S,E., Lecturer on Ophthabnic
Medicine and Sureery in Anderson's Col-
lege, Glasgow. With 10 Coloured Plates
and 157 Wood Engravings. Svo, ^\ Is.

The General Practitioner's
Guide to the Diseases and Injuries
of the Eye and Eyelids. By Lot;is
H. TosswiLL, B.A., M.B. Cantab,,
M.R.C.S., Su^eon to Ihe Exeter Eye
Infirmary. Fcap. 8vo, is. 5d.

H ints on Ophthalmic Out-Patient
Practice. By Charles Hicgens,
Ophthalmic Surgeon to Guy's Hospital.
Second Edition. Fcap. Svo, Js.

The Electro-Magnet,

And its Employment in Ophthalmic Sur-
gery. By Simeon Sneli., Ophthaliiuc
Su^eon to the Sheffield General In-
-* fitmary, &c. Crown 8vo, 3s. 6d. J^H

J. ,^ A. CHURCHILL'S RECENT WORKS.

\

The Student's Guide to Diseases

of the Eye. ByEDWARDNETTLE-iHIP,
F.R.C.S,, Ophthalmic Surgeon to St,
Thotnas's Hospital. Third Edition. Fcap.
Svo, with 150 Engravings and a !^et of
Coloured Papers iilusltating Coloui-Blind-

Manual of the Diseases of the

Eye. By Charles Macnamara,
F.R.C.S., Surgeon to Westminster Hos-
pital. Fourth Edition. Ciown Svo, with
4 Coloured Plates and 66 Engravings,
los. 6d.

A Manual of the Principles and
Practice of Ophthalmic Medicine
and Surgery. By T. Wharton
Jones, F.R.C.S., F.R.S. Third
Edition. Fcap. Svo, with 9 Coloured
Plates and 173 Engravings, us. 6d.

Glaucoma :

Its Causes, Symptoms, Patholc^, and
Treatment. By Priestlev Smith,

with Lithographic Plates,
Refraction of the Eye :

A Manual for -Students. ByGusTAVUS
■ IlAfiTRlDGE, F.R.C.S., Assistant Physi-
cian to the Royal Westminster Ophthalmic
Hospital. Crown Svo, with Llthi^aphic
Plate and 84 Woodcuts, 55.

Hare-Lip and Cleft Palate.

By Francis Mason, F.R.C.S., Sui^on
to St. Thomas's Hospital. Svo, with 66
Engravings, 6s.

By the same Author.

The Surgery of the Face.

8vo, ivith 100 Engravings, 7s. 6(1.
A Practical Treatise on Aural
Surgery. By H. MACNAt;GMTON
Jones, M.D., Professor of the Queen's
University in Irelatid, late Surgeon to the
Cork Ophthalmic and Aural Hospital.
Second Edition. Crown Svo, with 63
Engravings, 8s. 6d.

By the saiiit Author.

Atlas of Diseases of the Mem-
brana Tympani, In Coloured
Plates, containing 62 Figures, with Text,

Diseases and Injuries of the
Ear. By W.B. Dalbv,F.R.C.S., Aural
Surgeon to St. George's Hospital. Third
Edition. Crown 8vo, with Engravines,
7S. 6d. i. e '

Lectures on Syphilis of the

Larynx (Lesions of the Secondary and

/ntermediale Stages). By W. M. Whist-

LS.K, M.D., Physician to the Hospital

/or Diseases of the Throat. Post &vo. ^s.

Diseases of the Throat and

Nose : A Manual. By MoKELL Mac-
kenzie, M.D. Lond., Senior Physician,
to the Hospital for Diseases of the Throat,
Vol. I. Diseases of the Pharynx, Laryru^;
and Trachea. Post Svo, with 112 En-
gravings, I2S. 6d.

Vol. H. Diseases of the Nose and Naso*
Pharynx ; with a Section on Diseases ti
the (Esophagus. Post Svo, with 93 En-

gravings,

i. 6d.

Anther

■ Thyreocele :

''I

By iJie sam
Diphtheria :

Its Nature and Tre
Local Expressions.

Endemic Goitre i
Its E

Myxonlema, &c., and Treatment. ^^
William Robinson, M.D. Svo, 55.
Sore Throat :

Its Natnre, Varieties, and Treatmeob '
ByPHossER James, M.D,, Physician We,
the Hospital for Diseases of Che ThrtMl.
Fourth Edition. Post Svo, with Colonredtll
Plates and Engravings, 6s. 6d.

The Ear:

Its Anatomy, Physiolccy, and Diseasc8.J
By C. H. Burnett, Ajtl., M.D., Amatl
Surgeon to the Presbyterian Hospit^..
Philadelphia. Second Edition, Svo, with '
107 Engravings, 18s. (

A Treatise on Vocal Physio-
logy and Hygiene, with " '

reference to the Cultivation oe
servalion of the Voice. By C
Holmes, M.D., Physician to the Mob
cipal Throat and Eat Inlirmaiy. SeCoB.
Edition, with Engravings. Crown Svo
6s. 6d.

By the saiiu Author.
A Guide to the Use of the
Laryngoscope in General Prac-
tice. Crown Svo, with Engravings, zs.6d

A System of Dental Surgery.

Ky John Tomes, F.R.S., and C. S
Tomes, M.A., F.R.S. Third Editioa
Fcap. Svo, with many Engraving.

[In the /Vwl

Dental Anatomy, Human and

Comparative : AManual. ByCHARLW

S. Tome.';, M. A., F.R.S. Second EditioB.

Crown Svo, with 191 Engravings, ris. 6d. '

The Student's Guide to Dental

Anatomy and Surgery. By Hei
Sewill, M.R.C.S., L.D..S, Second
Edition. Fcap. 8vo, with 78 Engravings,

Mechanical Dentistry in Gold

and Vulcanite. By F. H. Balk-
will, L.D.S.R.C.S. Svo, with a Liibo-

tii^kic Plates and 57 Engravings, 1

Principles and Practice of Den-
tistry ; including Analomy, PhysioloEy,
Palholi^, Therapeutics, Denial Surgery,
and Mechanism. By Chapin A. Harris,
M.D., D.D.S. Revised and Edited by
Ferdinand J. S. G org as, A.M.,
M.D., D.D.S., Professnr in the Denial
Department of Marylanii University.
Eleventh Edition. 8vo, with 75a lUug-
tralions, 31s. 6d.

A Manual of Dental Mechanics.
By Oakley Coles, L.D.S.R.C.S.
Second Edition. Crown 8vo, with 140
Engravings, 7s. 6d,

By the same Author.

Deformities of the Mouth.

Third Edition. 8vo, with 83 Wood En-
gravings and 96 Drawings on Slone, 12s. 6d.

Notes on Dental Practice. By

HE.NHY C. QOINBV, L.D.S.R. C.S.I.
8vo, with 87 Engravings, 9s.

Elements of Dental Materia
Medlca and Therapeutit», iwlth
PharmacopCBia. By Jambs Stocken,
L.D.S.R.C.S., Pereirit Prizeman for
Materia Medica, anil Thomas Gadqks,
L.D.S. Eng. and Edin. Third Edition.
Fcap. 8vo, 7s. 6d.

Dental Medicine :

A Manual of Denial Materia Medica and
Therapeutics. By F. J. H. Goroas, A.M.,
M.D., D.D.S., Editor of "Harris's
Principles and Practice of Dentistry,"
Professor in the Dental Department of
Maryland University. Svo, 14B.

Lectures on Dermatology :

Delivered at the Royal College of Sur-
geons, by Sir Erasmus Wilson, F.R.S.
1870, 6s. ; 1871-73, 105. 6d. ; 1874-75,
los. 6d. ; 1S76-78, IDS. 6d.

£czema.

By McCall Anderson, M.D., Professor
of Clinical Medicine in the University of
Glasgow. Third Edition. Svo, with
Engravings, 7s. 6d.

Diseases of the Skin :

With an Analysis of 8,000 Consecutive
Cases and a Formulary. By L. D. BULK-
LEY, M.D., I'hysician for Skin Diseases at
the New York Hospital. Crown 8vo,6s.6d.

On Certain Rare Diseases of the
Skin. By Jonathan Hutchinson,
F.R.S., Senior Sui^eon to the London
Hospital, and to the Hospital for Diseases
of the Skin. Svo, los. 6d.

Diseases of the Skin :

A Practical Treatise for the Use of
Students and Praclilioners. By J. N.
HVDB,A.M.,M.D., Professor of Slan and
Venereal Diseases, Rush Medical College,
Chicago. 8vo, with 66 Engravings, 17s.

Parasites :

A Tteati.ie on Ihe Enlozoa of Man and
Animals, including some Account of the

EclOIOa. ByT.SPBNtERCOBBOMJ.M.D.,

F.R.S. 8vD, with 85 Engravings, 15s.

Atlas of Skin Dis<

By TiLHURV Fox, M.D., F.R.C.P.
With 71 Coloured Plates. Royal 4I0, half
morocco, £6 6s.

Leprosy in British Guiana.

ByJoHND.HiLLis,F.R.C.S.,M.R.I.A.,
Medical Superintendent of the Leper
Ayslum, British Guiana. Imp. Svo, with
33 Lithographic Coloured Plates and
Wood Engravings, £1 lis. 6d.

Certain Forms of Cancer,

With a New and Successful Mode of Treat-
ing it. By A. Mabsdbn, Senior Surgeon
to the Cancer Hospital. Second Edition.
Svo, with Coloured Plates, Ss. 6d.

Cancer of the Breast.

By Thomas W. Nunn, F.R.C.S., Con-
sulting Surgeon to the Middlesex Hos-
pital. 4tD, with 31 Coloured Plates, £3 3s.

On Cancer:

Its Allies, and other Tumours; withspedal
reference to their Medical and Surgical
Treatment. By F. A. Purcell, M.D.,
M.C., Sui^eon to the Cancer Hospital,
Bromplon. Svo, with 21 Engravings,

Sarcoma and Carcinoma :

Their Pathology, Diagnosis, and Treat-
ment. By Henry T. BuTLtN,F.R.C,S.,
Assistant Sui^eon to .St. Bartholomew's
Hospital. 8™, with 4 Plates, Ss.
By ihe same Author.

Malignant Disease of the La-
rynx (Sarcoma and Carcinoma).
Svo, with 5 Engravings, 55.

Clinical Notes on Cancer,

Its Etiology and Treatment ; with special
reference to the Heredity- Fallacy, and to
the Neurotic Origin of most Cases of
Alveolar Carcinoma. By Herbert L.
Sn-ow,M.D. Loud., Surgeon to theCancer
Hospital, Bromplon. Crown Svo, 3s. 6d.

Diseases of the Testis, Sperm-
atic Cord, and Scrotum. By
Thomas B. Curling, F.R.S., Consult-
ing Surgeon In the London Hospital-
Fourth Edition. Svo,withEngravings, 16s.

The Surgery of the Rectum.

By Henry Smith, Professor of Surgery
in King's College, Surgeon to the Hos-
pital. Fiflh Edition. Svo, 6s.

Lectures on the Surgical Dis-
orders of the Urinary Organs. By
Reginald HAt(RisoN,F.R.C.S.,Su[^eon
to the Liverpool Royal Infirmary. Second
Edition, with 48 Engravings. Svo, 12s. 6d.
By the same Author.

Lithotomy, Lithotrity, and the
Early Detection of Stone in the
Bladder ; with a description of a New
Method of Tapping the Bladder. "
with Engravings, 25. 6d.

.New J

f

u

J. & A. CHURCHILVS RECENT WORKS.

"!

Diseases of the Urinary Organs.
Clinical l.ectuies. By .Sir Henry
Thompson, F.R.C.S., Emeritus Pro-
fessor of Clinical Surgery in Univetiily
College. Seventh (Students') Edition.
Svo, with 84 Engiavings, is. 6d.
By the stain Author.

Diseases of the Prostate :

Fifth

Engravings,

Surgery of the Urinary Organs.

Some Impottanl points connected there-
with. Lectures delivered in Ihe R.C.S.
Svo, with 44 Etigcavings. Students'

Editi

;. 6d.

Also.

Practical Lithotomy and Litho-
trity; or. An InquiryinlolheBestModes
of Removing Stone from the Blaiider.
Third Edition. Svo, with 87 Engravings,

Also.

The Preventive Treatment of
Calculous Disease, and the Use of
Solvent Remedies. Second Edition
Fcap. 8vo, 2s. 6d.

Ahc.

Tumours of the Bladder :

Their Nature, Symptoms, and Surgical
Treatment. 8vo, with numerous lUustra-

Ako.
Stricture of the Urethra, and Uri-
nary Fistulaer their Patholi^y and Treat-
ment. Fourth Edition, Svo. [In the Press.

Hydrocele :

lis several Varieties and their Treatment.
By Samuel Osborn, late Surgical
Registrar to St. Thomas's Hospital.
Fcap. Svo, with Engravings, 3s.
By Ihe same Author.

Diseases of the Testis.

Fcap. 8vo, with Engravings, 3s. fid.
Fistula, Heemorrhoids, Painful
Ulcer, Stricture, Prolapsus, and
other Diseases of the Rectum ;
Their Diagnoas and Treatment. By
William Allingham, Su^eon to Si.
Mark's Hospital for Fislula. Fourth
Edition. Svo, with Engravings, 10s. 6d.
Diseases of the Rectum and
Anus. By W. Harrison Cripps,
F.R.C.S., Assistant Surgeon to Si. Bar-
tholomew's Hospital, &c. Svo, with 13
Lithc^raphic Plates and numerous Wood
Engravings, izs. 6d.
Pathology of the Urine.

Including a Complete Guide to its Analy-
sis. By J. L. W. Thudichum, M.D.,
F.R.C.P. Second Edition, rewritten and
eniaiged. Svo, with Engravings, 15s.

Student's Primer on the Urine. '

By J. Travis Whittaker. M.D., Clini-
cal Demonstrator at the KoyaJ Inlirmaij,
(jlasgow. With 16 Plates etched on
Copper. Post Svo, 4s. 6d.

Syphilis and Pseudo-syphilis.
By Alfked Cooper, F.R.C.S., Su^eon
to the Lock Hospital, to St. Mark's aod
Ihe West I.ondon Hospitals. Svo, icis.6d.

Genito-Urinary Organs, include
ing Syphilis ; A Practical Treatise oA
their Surgical Diseases, for Stadents and ,
Practitioners. By W. H. Van Buren,
M.D., and E. L. Keyes, M.D. Royal'.
Svo, with 140 Engraving, 21s. '

Lectures on Syphilis. i^

By Henrv Lee, Consulting Silicon to
St. George's Hrepital. Svo, los. '

Urinary and Reproductive Or>Ci<
gans : Their Functional Diseases. By
D. Campbell Black, M.D. Second '
Edition. Svo, los. ;

Coulson on Diseases of the
Bladder and Prostate Gland.

Sixth Edition. By Walter J. CoiilsOM,
Surgeon to the Lock Hospital and to SL
Peter's Hospital for Stone. Svo, l6s,

On Rupture of the Urinary Blad-
der. Based on the Records of more
than 300 Cases of the Affection. Bj ■
Walter Rivington, F.R.C.S., Presi-
dent of the Hunterian Society ; Surgeon 1
to the London Hospital. 8vo, 5s. 6d. <

The Reproductive Organs |

In Childhood, Youth, Adult Age, and Adrj<
vanced Life, considered in their Physio- '
tt^eal. Social, and Moral Relations. Br '
William Acton, M.R.C.S. Sixtt .
Edition. Svo, 12s. ,

The Medical Adviser in Life As-^

_, E. H.SlEVEKING,M.D.,

F.R.C.P. Second Edition. Crown8vo,6(. I
A Medical Vocabulary: I

An Explanation of all Terms and Fhrasei j
used in the various Departments of Me<he«li^
Science and Practice, their Derivalioui j
Meaning, Application, and Pronunciation. ,
ByR. U. Mayne, M.D., LL.D. Fiftfc. '
Edition. Fcap. Svo, los. 6d. 1

A Dictionary of Medical Science;^
Containing a concise Enplanalion of tin"
various Suhjects and Terms of Medicine .
&c. By ROHLEV DUNGLISON, M.D,r

LL.D. New Edition. Royal Svo, zSs.
Abridged Medical Accouot<
Books. The "Expedite" Method. By
J. Macnab, L.R.C.S.E. Index Led^tr.
Royal 4to., 155. Visiting List. Cloth,3K-
Leather, in Pocket-book form, with Pm-

Medical Education |

And Practice in ail parts of the WoiU,
By H. J. Hardwicke, M.D., M.R.C.P.-

Jupliiccincnta of U
a Nunng, ,

linthain on Diseases oflht R«l

ideiHiD(McC}ai>Eczeiti!l, ij

iBcaua or Ihe Han and Anna, B

G.) How la ArrESI Infeciioua Discs!
) on ObsiMric OKniiions, 5
on Di»!UES of WomitD, ;
IH m Medicine. B

JnSU H^^.h(

SrslcmUic BoUny, 7

Irnune" Topo^^ill^l'iimy. 3
Lndhur^t's AochyloEU, ri

Curvalares, &c., of tbe Spine, 11

Onhopiedic Suigtiy. n

^

Buikley'K EcicDU, ij
Buidctl'j Cotlage Hospiul!, j

PayHcspitils, s

Burnett OB the Ear, 11

BaiHnV Midwifery for Midwives, s

BntBn'l Uotigmnt DiscoK of cbe Larynx, i;

SoTcrana and Carcinoma, 13

Buuud'a DiBeucB of the Nervmu SyMEm, g
Cupcntei'i HuDun Phyiioloey, 4
Ckitcr (H. V.) on SpiriDum feyer, S
C^le/i Typihi^ F^tr, S
Chmerie' Fnctice of Medicine, S
ChA-l Outlines of Sunery, 10
Ocasttm'tLecIure!] on Mental Diseases, 5
Cobb^ on PiToniEB, 13
ColB' Dmtol Hechanics

feheM

Cooper'c S^kilu ^ .,

Cadm 00 DiHOHS of llic Bladder, 1.
COVMJ'S nteuei of the Uterus, Ovnnes, ftc, 6
Crippa' DiioHi of the Renun and Anus. 14
CtlBmeworth'i Manual of Nursing, 7

Short Manaal forMonlhly Nnrs.

CurlinE's Diieoses of the Testis, 13

Dllby^ Diseases and Injuries af the Ear, 12

DaJton'i Konian Pbyuology, 4

Day on Diseases of Children. 7

—^^ on Headaches, g

Dobeirs Lectures on Winter Cough. 3

Loss of W.' ■ -

Dungliscn's Medico] IHctionaty, [4
Ellis's Manual for Mothers, 6

of the Diseases of Children, 6

EAmet's GynEcology, 6

yaynr'a Chmau and Feven of India, 7

TVotricol X^ientery and Diamuea, 7

Fenwick's Chronic Atrophy of the Stomach, B

MadicolDiunoais, S

OutUnei oF Medical Treatment, S

Fwpuun's Practical Surgery, id

Frey't Hulology ar

Hordwicte's Medical Education, 14
Morley on Diseases of the Uver, q
Harris's Dentistry, u
Harrison's Lithotomy. IJlhotritj', &c, Ij

Surgical Disonlcrsor the Urinary Organs, 13

Honridge's Refraction of the Eye, 13
Heath's Injuries and Diseases of the Jaws ,0

— Human Osteology, 3

— Landmarks, i

s' (G.) Guide to Use of Laryngoscope, t'-
Vocal PhyHology and Hygiene, i

Hooper's Physician's VadE-Mecmn, B
Horton's Trd[»cal Disesss, B
Hutchinson's Clinical Snrpry, 11
— ■ — — Pedigree of Disdse, ir

es (P.) on Sore Ti

5'ft:. H.JFunciic

s (C. H.) and Sieveking's Patholc
s'(H. McNOAur-'" --

esof MembronaTympani,!?
W.J Ouhlhalrnic llfedicine and Surgery, iz

Leotntlon Syphilis, 14 '"' '^^' *

Lewis (Sevan) on the Hnman Brain, 4
Liveing's Me^m, Sick Headache, &c., g
London Hospital Reports, 2
Macdonald's<A.}Chronic Disease of the Heart,
Macdonajd'.i U- P-) Examination of Water and

McLeod's Operarive SurgetJ, 10

Mar^den's Certain Forms of Cancel
Mason on Hare- Up and aef) Palal

Mayne's Medical Voce buiary, 14

Middleso Hospital Repoits, 1
Mitchell's Diseases of the Nervous System
MooR'i Funily Medicine for India, 7

HeoUh-ReMtts for Trmical Inval

Morris' (H.) Anatomy of the Joints, 3
Mouat and Snell on Hospitals, s
Netileship's Diseases of (he Eye, 11
Nunn's CWer of the Bnast, 13
Ogston's Medical Jurisprudence, 4
Ophthalmic (Reyal LondonJHntpit
Ophthotniological Sodely's Transac
Oppert's Kmsuls, InSnnan' " '
Osbom DO Diseases of the Tf

Pkge's Injuries of the Spine, zz
Pftrkes' Practical Hygiene, 5
Pavy 00 DiabetesL ^

on Food and Dietetics, 9

Phannaoeutical Joornal, 3
niarmacopaaa of the Loodon Hoq>ital, ^
Phillips* Materia Medica and Therapeutics, 7
Pollock on Rheumatism,

Porritt's Intn-Thoracic Effusion, 8
Porcell on Cancer. 13
Pye-Smith's Syllabus of Physiology, 4
^uinb/s Notes on Dental Practice, 13
RamsboCham's Obstetrics, 6
Raye's Ambulance Handbook, zo
Reynolds' (J. J.) Diseases of Women, 6

Notes on Midwifery, 6

Rivington's Rupture of the Urinary Bladder, Z4
Robots* (C.) Manual of Anthrcnometry, 5

Detection of Colour^Bundness, 5

Roberts' (D. Lloyd) Practice of Mkiwifery, 5

Robinson s Endemic Goitre or Th3rreocele, la

Ross's Diseases of the Nervous System, 9

Roth on Dress : Its Sanitary Aspect, 4

Routh's Infiuit Feeding, 7

Royal College of Surgeons Museum Catalogues, a

Royle and Harl^s Materia Medica, 7

St. Bartholomew's Ho«>ital Reports, a

St. George's Hospital Reports, a

St. Thomas's Hospital^ Reports, a

Sanderson's Physiological Handbodc, 4

Sansom's Diseases of the Heart, 9

Savage on the Female Pelvic Organs, 6

Savres Orthopaedic Surgery, iz

Scnroeder's Manual of Midwifery, 6

Sevrill's Dental Anatomy, za

Sibson's Medical Anatomy, 3

Sieveking's Life Assurance, 14

Smith's (E.) Clinical Studies, 6

— — Disease in Children, 6

Wasting Diseasesof Infants and Children, 6

Smith's f Henry) Surgery of the Rectum, 13

Smith's (Heywood) Dvsmenorrhoea, 6

Smith (Priestley) on Glaucoma, za

Snell's Electro-Magnet in Ophthalmic Surgery, xz

Snow's Clinical Notes on Csincer, 13

Southam's Regional Suigery, zi

Sparks on the Riviera, 10

Squire's Companicm to the Pharmacopoeia^ 7

Phannacopoeias of London Hospitals, 7

Starkweather on the Law of Sex, 4

Steavenson's Electricity^ 10

Stills and Maisch's National Dispensatory, 7

Stimson on Fractures, it

Stocken's Dental Materia Medica and Therapeutics, 13

I N UKX^amtinuetL

Swain's Surcical Emavenaes, zo
SwavncTs Obstetric Afhansaa, 6
Tayws Medical Jurisprudence, 4

Poisons in relation to Medical Juriqnudeoce^

Teale's Dangers to Heakh, 5

Thompson's (Sir H.) CalciuoBS DiMiwe, X4

— — — — — ^^— Diseases of the Prostate. Z4

IXseasesoftfae Urinary Organs, 14

Lithotomy and Lithomty. 14

-^— — — ^^— — Stricture <rf the Urethra, 14

Suigery of the Urinary Organs, 14

Tumours of the Bladaer, 14

Thorowgood on Asthma, 8

; on Materia Medica and Ther^>eutics, 7

Thudichum's Pathology of the Urine^ 14
Tibbks' Medical and Sur^pcai Electricity, zo

— Map of Motor Pomts^ 10

Tidy and Woodman's Forensic Medicine, 4
TUt^s Change of Life, 6

Uterine Therapeutics, 6

Tomes' ^C. S.) Dental Anatomy, la
Tomes' y. and C. S.) Dental Siuigery, la
Tosswill s Diseases and Injuries of the Eye, xz
Tuke's Influence of the Mmd upon the Body, 5

Sleep- Walking and Hypnotism, 5

Van Buren on the Genito-Urinarv Organs, X4
Vintras on the Mineral Waters, &c, of France, 10
Virchow's Post-mortem Examinations, 4
Wagjstaffie's Human Osteology, 3

Waring's Indian Bazaar Medicines, 7
Warner's Guide to Medical Case-Taking, 8
Warren's Hernia and Rupture, ix '
Waters' (A. T. H.) Diseases of the Chest, 8
Waters 0- H.) on Fits, jj
WeUs (Spencer) Abdominal Tumours, 6

on Ovarian and Uterine Tumours, 6

West and Duncan's Diseases of Women, 6

West (S.) How to Examine the Chest, 8
Whistler's Syphilis of the Larynx, xa
Whittaker's Primer on the Unne, X4
Wilks' Diseases of the Nervous System, 9
Wilks and Moxon's Pathological Anatomy, 4
Wilson's (Sir E.) Anatomist^ Vade-Mecum, 3

Lectures on Dermatology, 13

Wilson's (G.) Handbook of Hygiene, ^

Healthy Life and Dwelkngs, 5

Wilson's (W. S.) Ocom as a Health-Resort, xo
Wolfe's Diseases and Injuries of the Eye, zx
Year Book of Pharmacy, a
Yeo's (G. F.) Manual of Physiology, 4
Yeo's (J. B.) O>ntagiousness of Pulmonary Consump-
• tion, 8
Zander Institute Mechanical Exercises, 10

The following Catalogues issued by J. & A. Churchill will be forwarded

post free on application : —

A. J, ^ A. ChurchiWs General List of about 650 works on Anatomy ^
Physiology y Hygiene^ Midwifery ^ Materia Medica^ Medicine^ Surgery ^ Chemistry ^
Botany^ 4"^., g*^., with a complete Index to their Subjects^ for easy referenu,
N.B. — This List includes B, C, & D.

B. Selection from J. 8f A, ChurchilVs General Listy comprising all recent
Works published by them on the Art and Science of Medicine,

C. J, ^ A, ChurchilVs Catcdogue of Text Books specially arranged for Students.

D. A selected and descriptive List of J. ^ A. ChurchilVs Works on
Chemistry^ Materia Medica^ Pharmacy, Botany, Photography, Zoology, the
Microscope, and other branches of Science,

E. The Half-yearly List of New Works and New Editions published by
J, 8f A, Churchill during the previous six months, together with particulars of
the Periodicals issued from their House,

[Sent in January and July of each year to every Medical Practitioner in the United
Kingdom whose name and address can be ascertained. A large number are
also sent to the United States of America, Continental Europe, India, and the
Colonies.]

America. — J, ^ A, Churchill being in constant communication with
various publishing houses in Boston, New York, and Philadelphia, are
able, notwithstanding the absence of international copyright, to conduct
neg-otiations favourable to English Authors,

LONDON: NEVJ BXS^lAl^OtO^ ^T^SK^,

__ J nr* «xi*> - . «s-